Journal articles on the topic 'CA3 pyramidal neurons'
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1
Dasari, Sameera, and Allan T. Gulledge. "M1 and M4 Receptors Modulate Hippocampal Pyramidal Neurons." Journal of Neurophysiology 105, no. 2 (February 2011): 779–92. http://dx.doi.org/10.1152/jn.00686.2010.
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Acetylcholine (ACh), acting at muscarinic ACh receptors (mAChRs), modulates the excitability and synaptic connectivity of hippocampal pyramidal neurons. CA1 pyramidal neurons respond to transient (“phasic”) mAChR activation with biphasic responses in which inhibition is followed by excitation, whereas prolonged (“tonic”) mAChR activation increases CA1 neuron excitability. Both phasic and tonic mAChR activation excites pyramidal neurons in the CA3 region, yet ACh suppresses glutamate release at the CA3-to-CA1 synapse (the Schaffer–collateral pathway). Using mice genetically lacking specific mAChRs (mAChR knockout mice), we identified the mAChR subtypes responsible for cholinergic modulation of hippocampal pyramidal neuron excitability and synaptic transmission. Knockout of M1 receptors significantly reduced, or eliminated, most phasic and tonic cholinergic responses in CA1 and CA3 pyramidal neurons. On the other hand, in the absence of other Gq-linked mAChRs (M3 and M5), M1 receptors proved sufficient for all postsynaptic cholinergic effects on CA1 and CA3 pyramidal neuron excitability. M3 receptors were able to participate in tonic depolarization of CA1 neurons, but otherwise contributed little to cholinergic responses. At the Schaffer–collateral synapse, bath application of the cholinergic agonist carbachol suppressed stratum radiatum–evoked excitatory postsynaptic potentials (EPSPs) in wild-type CA1 neurons and in CA1 neurons from mice lacking M1 or M2 receptors. However, Schaffer–collateral EPSPs were not significantly suppressed by carbachol in neurons lacking M4 receptors. We therefore conclude that M1 and M4 receptors are the major mAChR subtypes responsible for direct cholinergic modulation of the excitatory hippocampal circuit.
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Lamsa, Karri, J. Matias Palva, Eva Ruusuvuori, Kai Kaila, and Tomi Taira. "Synaptic GABAA Activation Inhibits AMPA-Kainate Receptor–Mediated Bursting in the Newborn (P0–P2) Rat Hippocampus." Journal of Neurophysiology 83, no. 1 (January 1, 2000): 359–66. http://dx.doi.org/10.1152/jn.2000.83.1.359.
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The mechanisms of synaptic transmission in the rat hippocampus at birth are assumed to be fundamentally different from those found in the adult. It has been reported that in the CA3-CA1 pyramidal cells a conversion of “silent” glutamatergic synapses to conductive α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) synapses starts gradually after P2. Further, GABA via its depolarizing action seems to give rise to grossly synchronous yet slow calcium oscillations. Therefore, GABA is generally thought to have a purely excitatory rather than an inhibitory role during the first postnatal week. In the present study field potential recordings and gramicidin perforated and whole cell clamp techniques as well as K+-selective microelectrodes were used to examine the relative contributions of AMPA and GABAA receptors to network activity of CA3-CA1 pyramidal cells in the newborn rat hippocampus. As early as postnatal day( P 0–P2), highly coherent spontaneous firing of CA3 pyramidal cells was seen in vitro. Negative-going extracellular spikes confined to periodic bursts (interval 16 ± 3 s) consisting of 2.9 ± 0.1 spikes were observed in stratum pyramidale. The spikes were accompanied by AMPA-R–mediated postsynaptic currents (PSCs) in simultaneously recorded pyramidal neurons (7.6 ± 3.0 unitary currents per burst). In CA1 pyramidal cells synchronous discharging of CA3 circuitry produced a barrage of AMPA currents at >20 Hz frequencies, thus demonstrating a transfer of the fast CA3 network activity to CA1 area. Despite its depolarizing action, GABAA-R–mediated transmission appeared to exert inhibition in the CA3 pyramidal cell population. The GABAA-R antagonist bicuculline hypersynchronized the output of glutamatergic CA3 circuitry and increased the network-driven excitatory input to the pyramidal neurons, whereas the GABAA-R agonist muscimol (100 nM) did the opposite. However, the occurrence of unitary GABAA-R currents was increased after muscimol application from 0.66 ± 0.16 s−1 to 1.43 ± 0.29 s−1. It was concluded that AMPA synapses are critical in the generation of spontaneous high-frequency bursts in CA3 as well as in CA3-CA1 transmission as early as P0–P2 in rat hippocampus. Concurrently, although GABAA-R–mediated depolarization may excite hippocampal interneurons, in CA3 pyramidal neurons it can restrain excitatory inputs and limit the size of the activated neuronal population.
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Zhuravleva, Z. N., V. N. Saifullina, and C. I. Zenchenko. "Morphometric Analysis of Hippocampal Pyramidal Neuronsin situand in Grafts Developing in the Anterior Eye Chambers of Young and Aged Wistar Rats." Journal of Neural Transplantation and Plasticity 6, no. 1 (1997): 49–57. http://dx.doi.org/10.1155/np.1997.49.
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We performed a morphometric analysis of the somatic and nuclear areas in the pyramidal neurons of the hippocampal fields CA1 and CA3in situand in grafts developing for six weeks in the anterior eye chambers of young (3-to-9 wk.) and of aged (18-to-19.5 mos.) Wistar rats. The mean areas of the CA1 pyramidal somata and nuclei were significantly decreased in the aged animalsin situ. The mean parameters of the CA3 pyramidal neurons were not changed, although their distribution was different (bimodalversusunimodal in the young animals). In both groups of recipients, the areas of CA1 neurons and of their nuclei were significantly larger in the grafted tissue than those foundin situ. The areas of CA3 neurons did not show any difference in aged recipients and demonstrated only slight hypertrophy in young recipients. We concluded that the area sizes of the pyramidal cell bodies and nuclei in CA1 neurons are more sensitive than those of CA3 neurons to both aging and transplantation. The age of recipients did not significantly influence the growth and development of grafted pyramidal cells.
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Debanne, D., N. C. Guerineau, B. H. Gahwiler, and S. M. Thompson. "Physiology and pharmacology of unitary synaptic connections between pairs of cells in areas CA3 and CA1 of rat hippocampal slice cultures." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1282–94. http://dx.doi.org/10.1152/jn.1995.73.3.1282.
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1. Paired intracellular recordings were made in rat hippocampal slice cultures, with the use of either sharp microelectrodes or the whole cell configuration of the patch-clamp technique. Unitary synaptic connections were studied between pyramidal and nonpyramidal cells within and between areas CA1 and CA3. 2. Monosynaptic excitatory synaptic responses between CA3 pyramidal neurons were found in 56% of cell pairs (n = 91, 28 postsynaptic cells). Monosynaptic connections from a CA3 cell to a CA1 cell were observed in 76% of cell pairs (n = 125, 26 postsynaptic cells), but from CA1 to CA3 neurons in only 8% of cell pairs (n = 13, 13 postsynaptic cells). Monosynaptic excitatory connections were found in only 16% of CA1/CA1 cell pairs (n = 25, 10 postsynaptic cells). 3. Disynaptic inhibition was commonly observed between CA3 cell pairs (43%), but rarely found between CA3-CA1 pyramidal cell pairs (2%). In 50% of CA3 pyramidal cell pairs, synchronous inhibitory postsynaptic potentials (IPSPs) in both cells could be triggered by an action potential in one pyramidal cell. Reciprocal monosynaptic connections were found between 75% of interneuron and pyramidal cell pairs within area CA3. 4. The latency of monosynaptic CA3- to CA1-cell responses was significantly longer than for responses between two CA3 cells. Within area CA3 the latencies for inhibitory synaptic responses between interneurons and pyramidal cells were significantly shorter than those for excitatory responses between pyramidal cells. Monosynaptic excitatory postsynaptic potentials (EPSPs) in interneurons had a significantly shorter time-to-peak than those recorded in pyramidal neurons. 5. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX)- and D-2-amino-5-phosphonovalerate (AP5)-sensitive components were identified in unitary monosynaptic EPSPs in CA3-CA3 and CA3-CA1 pyramidal cell pairs. The CNQX-sensitive component had a mean time-to-peak and duration of 6.2 +/- 0.3 (SE) ms and 61.2 +/- 2.0 ms, respectively, and an amplitude of approximately 1 mV (n = 93). The AP5-sensitive component of EPSPs was only detected when the cell was depolarized with respect to the resting potential, had a mean time-to-peak of 41 +/- 5 ms and duration of 121 +/- 11 ms (n = 6), and increased in amplitude with postsynaptic depolarization. 6. Unitary monosynaptic IPSPs between an interneuron and a pyramidal cell had a mean amplitude of approximately 1 mV and were fully blocked by gamma-aminobutyric acid-A (GABAA) receptor antagonists (n = 3). 7. Unitary inhibitory responses were found only within, but not between, areas CA3 or CA1.(ABSTRACT TRUNCATED AT 400 WORDS)
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Kirino, Takaaki, Hugh P. C. Robinson, Akiko Miwa, Akira Tamura, and Nobufumi Kawai. "Disturbance of Membrane Function Preceding Ischemic Delayed Neuronal Death in the Gerbil Hippocampus." Journal of Cerebral Blood Flow & Metabolism 12, no. 3 (May 1992): 408–17. http://dx.doi.org/10.1038/jcbfm.1992.58.
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Slice preparations were made from the hippocampus of gerbils after 5 min of ischemia by carotid artery occlusion and the membrane properties of pyramidal neurons were examined. A majority of CA1 neurons lost the capacity for long-term potentiation following tetanic stimulation of the input fibers. CA3 pyramidal neurons, in contrast, preserved responses similar to those in the normal gerbil. Following ischemia, CA1 pyramidal neurons showed increased spontaneous firing that was highly voltage dependent and was blocked by intracellular injection of the Ca2+ chelator, EGTA. Thirty-five percent of CA1 neurons showed an abnormal slow oscillation of the membrane potential after 24 h following ischemia. Intracellular injection of GTPγS or IP3 produced facilitation of the oscillations followed by irreversible depolarization. Our results indicate that ischemia-damaged CA1 neurons suffer from abnormal Ca2+ homeostasis, involving IP3-induced liberation of Ca2+ from internal stores.
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Lopez-Santiago, Luis F., Yukun Yuan, Jacy L. Wagnon, Jacob M. Hull, Chad R. Frasier, Heather A. O’Malley, Miriam H. Meisler, and Lori L. Isom. "Neuronal hyperexcitability in a mouse model of SCN8A epileptic encephalopathy." Proceedings of the National Academy of Sciences 114, no. 9 (February 13, 2017): 2383–88. http://dx.doi.org/10.1073/pnas.1616821114.
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Patients with early infantile epileptic encephalopathy (EIEE) experience severe seizures and cognitive impairment and are at increased risk for sudden unexpected death in epilepsy (SUDEP). EIEE13 [Online Mendelian Inheritance in Man (OMIM) # 614558] is caused by de novo missense mutations in the voltage-gated sodium channel gene SCN8A. Here, we investigated the neuronal phenotype of a mouse model expressing the gain-of-function SCN8A patient mutation, p.Asn1768Asp (Nav1.6-N1768D). Our results revealed regional and neuronal subtype specificity in the effects of the N1768D mutation. Acutely dissociated hippocampal neurons from Scn8aN1768D/+ mice showed increases in persistent sodium current (INa) density in CA1 pyramidal but not bipolar neurons. In CA3, INa,P was increased in both bipolar and pyramidal neurons. Measurement of action potential (AP) firing in Scn8aN1768D/+ pyramidal neurons in brain slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1 but not in CA3 hippocampal or layer II/III neocortical neurons. The maximum spike frequency evoked by depolarizing current injections in Scn8aN1768D/+ CA1, but not CA3 or neocortical, pyramidal cells was significantly reduced compared with WT. Spontaneous firing was observed in subsets of neurons in CA1 and CA3, but not in the neocortex. The EAD-like waveforms of Scn8aN1768D/+ CA1 hippocampal neurons were blocked by tetrodotoxin, riluzole, and SN-6, implicating elevated persistent INa and reverse mode Na/Ca exchange in the mechanism of hyperexcitability. Our results demonstrate that Scn8a plays a vital role in neuronal excitability and provide insight into the mechanism and future treatment of epileptogenesis in EIEE13.
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Muller, W., and U. Misgeld. "Picrotoxin- and 4-aminopyridine-induced activity in hilar neurons in the guinea pig hippocampal slice." Journal of Neurophysiology 65, no. 1 (January 1, 1991): 141–47. http://dx.doi.org/10.1152/jn.1991.65.1.141.
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1. Paired extra- and intracellular recording was used to study the activity of neurons in the dentate hilus and their interaction with CA3/CA4 pyramidal neurons and granule cells during picrotoxin- or 4-aminopyridine (4-AP)-induced rhythmical activity in the guinea pig hippocampal slice. 2. Picrotoxin induced synchronous repetitive population spikes in the CA3, CA4, and hilar region, but no extracellular activity in the granule cell layer. 4-AP induced rhythmically occurring positive field-potential waves in the CA3, CA4, and granular layer coincident to negative/positive field potentials in the hilus. 3. Picrotoxin-induced activity originated in the CA3 area and subsequently appeared in the CA4 and hilar region, whereas 4-AP-induced activity appeared simultaneously in all subfields. 4. Blockade of fast glutamatergic excitation by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) blocked the picrotoxin-induced activity but not the 4-AP-induced activity. 5. Focal application of tetrodotoxin (TTX) between area CA3 and CA4 blocked picrotoxin-induced activity in the CA4 and hilar region but decoupled 4-AP-induced activity in the CA3 area. 6. Under intracellular recording, picrotoxin induced bursts in CA3, CA4, and hilar neurons but K-dependent slow IPSPs in granule cells. 4-AP induced rhythmically occurring burst in hilar neurons synchronous to Cl- and K-dependent IPSPs in CA3, CA4, and granule cells. 7. Comparison of picrotoxin- and 4-AP-induced rhythmical burst activity reveals that many hilar neurons are excited by CA3/CA4 pyramidal neurons in addition to the well-known excitation by granule cells and perforant path fibers, and that, in turn, many hilar neurons inhibit CA3, CA4, and granule cells.
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Shcherbak, N. S., G. Yu Yukina, A. G. Gurbo, E. G. Sukhorukova, A. G. Sargsian, V. V. Thomson, and M. M. Galagudza. "Morphofunctional state of microglia and hippocampal neurons in aged rats after anesthesia with chloral hydrate." Regional blood circulation and microcirculation 21, no. 3 (October 12, 2022): 64–71. http://dx.doi.org/10.24884/1682-6655-2022-21-3-64-71.
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Introduction. Successful translating of the fundamental research results into clinical practice is determined by a sufficiently large number of components, including the age of experimental animals and the anesthesia used. Chloral hydrate is often used as an anesthetic in preclinical studies, while its effect on the morphofunctional characteristics of the hippocampus in aged animals remains unexplored, which can lead to significant distortion and incorrect interpretation of the obtain results. Objective – morphofunctional assessment of the neurons and microglia in the layers of CA1, CA2, CA3 and CA4 fields of the hippocampus in aged rats anesthetized with chloral hydrate. Materials and methods. Male Wistar rats at the age of 24 months were anesthetized with chloral hydrate (400 mg/kg). In the early (2 days) period after chloral hydrate anesthesia, the morphofunctional state of neurons and the reaction of microglia were qualitatively and quantitatively assessed by histological, immunohistochemical, and morphometric analysis in the marginal, pyramidal, and molecular layers of fields CA1, CA2, CA3, and CA4 of the hippocampus. Results. 48 hours after 24-month-old Wistar rats were anesthetized with chloral hydrate, changes in the morphofunctional state of the pyramidal layer of the hippocampus were shown to be characterized by a significant decrease in the number of neurons in fields CA1 and CA3 with two nucleoli by 42 and 54 %, respectively, and a decrease in the width of the layer of fields CA1 and CA3 and CA4 by 27, 29 and 21 %, respectively, compared with similar indicators in the control group (P<0.05). In all layers of fields CA1, CA2, CA3 and CA4 of hippocampus, microglia reacted by the transformation of Iba-1-positive microgliocytes body and processes and a significant increase of the Iba-1 protein expression compared to the animals without administration of chloral hydrate (P<0.05). Conclusions. A single chloral hydrate dose administration necessary to anesthetized the aged Wistar rats without model surgery leads to morphofunctional changes in neurons in the most vulnerable fields of the hippocampus with simultaneous activation of microglia in all fields. This circumstance must be taken into account when conducting basic research and preclinical studies.
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Wang, Jun, Mark F. Yeckel, Daniel Johnston, and Robert S. Zucker. "Photolysis of Postsynaptic Caged Ca2+ Can Potentiate and Depress Mossy Fiber Synaptic Responses in Rat Hippocampal CA3 Pyramidal Neurons." Journal of Neurophysiology 91, no. 4 (April 2004): 1596–607. http://dx.doi.org/10.1152/jn.01073.2003.
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The induction of mossy fiber-CA3 long-term potentiation (LTP) and depression (LTD) has been variously described as being dependent on either pre- or postsynaptic factors. Some of the postsynaptic factors for LTP induction include ephrin-B receptor tyrosine kinases and a rise in postsynaptic Ca2+ ([Ca2+]i). Ca2+ is also believed to be involved in the induction of the various forms of LTD at this synapse. We used photolysis of caged Ca2+ compounds to test whether a postsynaptic rise in [Ca2+]i is sufficient to induce changes in synaptic transmission at mossy fiber synapses onto rat hippocampal CA3 pyramidal neurons. We were able to elevate postsynaptic [Ca2+]i to approximately 1 μm for a few seconds in pyramidal cell somata and dendrites. We estimate that CA3 pyramidal neurons have approximately fivefold greater endogenous Ca2+ buffer capacity than CA1 neurons, limiting the rise in [Ca2+]i achievable by photolysis. This [Ca2+]i rise induced either a potentiation or a depression at mossy fiber synapses in different preparations. Neither the potentiation nor the depression was accompanied by consistent changes in paired-pulse facilitation, suggesting that these forms of plasticity may be distinct from synaptically induced LTP and LTD at this synapse. Our results are consistent with a postsynaptic locus for the induction of at least some forms of synaptic plasticity at mossy fiber synapses.
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Migliore, M., E. P. Cook, D. B. Jaffe, D. A. Turner, and D. Johnston. "Computer simulations of morphologically reconstructed CA3 hippocampal neurons." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1157–68. http://dx.doi.org/10.1152/jn.1995.73.3.1157.
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1. We tested several hypotheses with respect to the mechanisms and processes that control the firing characteristics and determine the spatial and temporal dynamics of intracellular Ca2+ in CA3 hippocampal neurons. In particular, we were interested to know 1) whether bursting and nonbursting behavior of CA3 neurons could be accounted for in a morphologically realistic model using a number of the known ionic conductances; 2) whether such a model is robust across different cell morphologies; 3) whether some particular nonuniform distribution of Ca2+ channels is required for bursting; and 4) whether such a model can reproduce the magnitude and spatial distribution of intracellular Ca2+ transients determined from fluorescence imaging studies and can predict reasonable intracellular Ca2+ concentration ([Ca2+]i) distribution for CA3 neurons. 2. For this purpose we have developed a highly detailed model of the distribution and densities of membrane ion channels in hippocampal CA3 bursting and nonbursting pyramidal neurons. This model reproduces both the experimentally observed firing modes and the dynamics of intracellular Ca2+. 3. The kinetics of the membrane ionic conductances are based on available experimental data. This model incorporates a single Na+ channel, three Ca2+ channels (CaN, CaL, and CaT), three Ca(2+)-independent K+ channels (KDR, KA, and KM), two Ca(2+)-dependent K+ channels (KC and KAHP), and intracellular Ca(2+)-related processes such as buffering, pumping, and radial diffusion. 4. To test the robustness of the model, we applied it to six different morphologically accurate reconstructions of CA3 hippocampal pyramidal neurons. In every neuron, Ca2+ channels, Ca(2+)-related processes, and Ca(2+)-dependent K+ channels were uniformly distributed over the entire cell. Ca(2+)-independent K+ channels were placed on the soma and the proximal apical dendrites. For each reconstructed cell we were able to reproduce bursting and nonbursting firing characteristics as well as Ca2+ transients and distributions for both somatic and synaptic stimulations. 5. Our simulation results suggest that CA3 pyramidal cell bursting behavior does not require any special distribution of Ca(2+)-dependent channels and mechanisms. Furthermore, a simple increase in the Ca(2+)-independent K+ conductances is sufficient to change the firing mode of our CA3 neurons from bursting to nonbursting. 6. The model also displays [Ca2+]i transients and distributions that are consistent with fluorescent imaging data. Peak [Ca2+]i distribution for synaptic stimulation of the nonbursting model is broader when compared with somatic stimulation. Somatic stimulation of the bursting model shows a broader distribution in [Ca2+]i when compared with the nonbursting model.(ABSTRACT TRUNCATED AT 400 WORDS)
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Klee, R., E. Ficker, and U. Heinemann. "Comparison of voltage-dependent potassium currents in rat pyramidal neurons acutely isolated from hippocampal regions CA1 and CA3." Journal of Neurophysiology 74, no. 5 (November 1, 1995): 1982–95. http://dx.doi.org/10.1152/jn.1995.74.5.1982.
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1. The properties of voltage-gated potassium currents were studied in acutely isolated rat hippocampal pyramidal cells from area CA1 and CA3 at postnatal ages of day 6-8, 9-14, and 26-29 (P6-8, P9-14, and P26-29) with the use of the whole cell version of the patch-clamp technique. 2. The outward current pattern of all cells under investigation could be separated in a fast transient A current (IA) and a delayed rectifier-like current (IK). 3. In both preparations, IA activated and inactivated rapidly. Vh describing steady-state inactivation was -84.5 mV in CA3 cells and -85.5 mV in CA1 cells. The activation behavior was characterized by Vh = -23.8 mV in CA3 cells and -27.2 mV in CA1 cells. The removal of inactivation was monoexponential both in CA1 and CA3 neurons with time constants of 32.1 and 28.5 ms, respectively. IA was insensitive to tetraethylammonium (TEA), dendrotoxin (300 nM), and mast cell degranulating peptide (200 nM), but could be blocked with 5 mM 4-aminopyridine (4-AP) by approximately 80%. In both preparations, A currents did not depend on Ca2+ influx. 4. Delayed rectifier currents (IK) in CA1 and CA3 pyramidal neurons decayed along a double exponential time course. Steady-state inactivation was described by Vh = -79.5 mV in CA3 cells and -76.0 mV in CA1 cells. The activation curves were characterized by midpoints of -3.8 mV in CA3 cells and of -1.4 mV in CA1 cells. The removal of inactivation was monoexponential in CA1 and CA3 neurons with time constants of 210.3 and 202.4 ms, respectively. All kinetic properties were identical for the differentially decaying components of IK. In CA1 cells IK was blocked by TEA at +30 mV with an IC50 of 0.98 mM. In CA3 cells the corresponding IC50 value was 1.05 mM. About 20% of IK were insensitive to TEA. IK was partially blocked by approximately 30% with 100 microM 4-AP. Mast cell degranulating peptide (100-200 nM) and dendrotoxin (50-300 nM) had no effect on IK. 6. Perfusion of charybdotoxin (30 nM), Cd2+ (300 microM), La3+ (10 microM), or Ca(2+)-free solutions resulted in the isolation of a small noninactivating outward current component. Around 10% of IK appeared to be Ca2+ dependent in CA1 neurons. In CA3 pyramidal cells Ca(2+)-dependent outward currents seemed to be somewhat larger with approximately 20%. 7. In CA1 as well as in CA3 cells, the kinetic and pharmacological properties of IA and IK remained stable during postnatal development. However, the contribution of IA and IK to the whole cell current varied with age. IA was more prominent in CA1 cells of age group P6-8 than in age-matched CA3 cells. CA3 cells had smaller A currents and larger delayed rectifier currents than CA1 pyramidal cells. Current densities of IA and IK were analyzed during development to assess changes in the expression of these currents. With increasing postnatal age, the expression of IA was downregulated in both preparations. This effect was more pronounced in CA3 than in CA1 cells. In contrast, IK was upregulated during the same developmental period. This increase in the expression of IK was with approximately 300% much larger in CA1 cells than in CA3 cells with only approximately 50%.
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Shokunbi, M. T., F. E. Olopade, O. M. Femi-Akinlosotu, and E. O. Ajiboye. "Pyramidal cell morphology and cell death in the hippocampus of adult mice with experimentally induced hydrocephalus." Nigerian Journal of Paediatrics 47, no. 4 (August 28, 2020): 298–304. http://dx.doi.org/10.4314/njp.v47i4.1.
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Background: Hippocampus is a neural structure in the temporal lobe that plays a crucial role in learning and memory. Cognitive impairment with learning disabilities is a common feature in hydrocephalus and is more prominent in adult-onset hydrocephalus. The aim of this study is to describethe morphological alterations in the pyramidal cells of the hippocampus of adult hydrocephalic mice.
Method: Hydrocephalus was induced in adult albino mice by intra-cisternal injection of kaolin suspension (250 mg/ml in sterile water). They were sacrificed 7, 14 and 21 days post-induction. Morphological analysis was carried out on hematoxylin and eosinstained coronal sections of the hippocampus: the pyramidal neurons (normal and pyknotic) in the CA1 and CA3 subregions were counted and the pyknotic index (PI) was calculated. The somatic and dendritic features of Golgistained pyramidal neurons were examined by light microscopy in both hydrocephalic and control mice.
Result: The PI was significantly greater in the CA1 region of the hippocampus in the hydrocephalic groups compared to the agematched controls. The dendritic processes of pyramidal neurons in the CA1 region were fewer with shorter terminal branches in the hydrocephalic mice than in controls; this was pronounced at 7 days post-induction. In the CA3 region, there was no difference in dendritic arborization between hydrocephalic and control mice.
Conclusion: Acute adult-onset hydrocephalus was associated with increased pyknosis and reduced dendritic arborization in hippocampal pyramidal cells in the CA1 but not CA3 region.
Keywords: Hippocampal pyramidal cell, Hydrocephalus, Pyknotic index, Golgi stain
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Thompson, L. T., J. R. Moyer, and J. F. Disterhoft. "Transient changes in excitability of rabbit CA3 neurons with a time course appropriate to support memory consolidation." Journal of Neurophysiology 76, no. 3 (September 1, 1996): 1836–49. http://dx.doi.org/10.1152/jn.1996.76.3.1836.
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1. The excitability of CA3 pyramidal neurons was assessed with intracellular recordings in hippocampal slices from behaviorally naive rabbits. CA3 pyramidal neurons had large (-13.1 +/- 0.3 mV; mean +/- SE) postburst afterhyperpolarization (AHPs) and exhibited robust spike-frequency adaptation (accommodation) to prolonged (800-ms) depolarizing current injection at resting potentials of -68 mV. AHP and accommodation measures differed in scale but not in kind from those obtained in stable recordings from CA1 pyramidal neurons in the same slices or from the same rabbits, with CA3 neurons having larger longer AHPs but fewer spikes during accommodation. 2. Groups of rabbits were trained in a simple, associative-learning task, trace eye-blink conditioning, which required an intact hippocampus for successful acquisition. Memory consolidation in this task also involves the hippocampus, whereas long-term retention of the learned response does not. The time course and magnitude of learning-specific changes in excitability were assessed in 201 CA3 pyramidal neurons. 3. Learning increased the excitability of CA3 pyramidal neurons soon after acquisition (within 1-24 h). The mean postburst AHP was reduced to approximately half (-6.4 +/- 0.3 mV) the basal amplitude of the AHP observed in naive controls. The area and duration of the postburst AHP similarly were reduced. Approximately half of all pyramidal neurons tested soon after learning exhibited significantly reduced AHPs, whereas none exhibited enhanced AHPs. 4. Trace conditioning also reduced accommodation of CA3 pyramidal neurons 1-24 h after learning. Neurons from successfully trained rabbits fired significantly more action potentials (5.6 +/- 1.5) in response to prolonged depolarization than did neurons from naive controls (4.1 +/- 0.2). The magnitude of the learning-specific change in accommodation was less than that for the AHP. Approximately 45% of neurons tested exhibited significantly reduced accommodation soon after learning. 5. Both learning-specific changes in CA3 increased neuronal excitability. Both changes were highly time dependent. AHPs were reduced maximally 1-24 h after learning, then increased, returning to basal (naive) levels within 7 days and remaining basal thereafter. The decay rate of accommodation to basal levels preceded that of the AHP by several days. 6. Other membrane properties, including action potential characteristics, resting potential, and input resistance, were unchanged by learning. The restriction of the observed changes to two interrelated measures of excitability concurs with earlier reports that learning-specific changes in the mammalian hippocampus are linked to changes in a limited number of membrane conductances. 7. Learning, not long-term memory or performance of the learned behavior, was linked to the excitability changes. Neurons from rabbits that failed to acquire the task after considerable training exhibited no excitability changes. Neurons from pseudoconditioned rabbits were indistinguishable from neurons of behaviorally naive controls. Finally, neurons from rabbits that explicitly demonstrated long-term retention of the conditioned response were indistinguishable from those of naive controls. 8. Behavioral changes persisted for extremely long periods, but the observed changes in hippocampal excitability were transient and greatest soon after learning. Excitability was enhanced for a period of a few days, a period demonstrated in other eyeblink studies to be required for memory consolidation. Because hippocampal excitability then returned to basal levels but memory of the learned task persisted, postconsolidation memory traces (the "engram") must be extrahippocampal.
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Jaffe, David B., and Thomas H. Brown. "Calcium Dynamics in Thorny Excrescences of CA3 Pyramidal Neurons." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 10–18. http://dx.doi.org/10.1152/jn.1997.78.1.10.
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Jaffe, David B. and Thomas H. Brown. Calcium dynamics in thorny excrescences of CA3 pyramidal neurons. J. Neurophysiol. 78: 10–18, 1997. Confocal laser scanning microscopy was used to visualize Ca2+ transients in a particular type of dendritic spine, known as a thorny excrescence, in hippocampal CA3 pyramidal neurons. These large excrescences or thorns, which serve as the postsynaptic target for the mossy-fiber synaptic inputs, were identified on the basis of their location, frequency, and size. Whole cell recordings were made from superficial CA3 pyramidal neurons in thick hippocampal slices with the use of infrared video microscopy; cells with proximal apical dendrites close to the surface of the slice were selected. Changes in intracellular Ca2+ levels were monitored by imaging changes in fluorescence of the dyes Calcium Green-1 and Fluo-3. Dual-emission fluorescence imaging was also employed with the use of a combination of Fluo-3 and the Ca2+insensitive dye seminaphthorhodafluor-1. This method was used todecrease the potential influence of background fluorescence on the calculated changes in intracellular Ca2+ concentration ([Ca2+]i). Somatic depolarization produced increases in [Ca2+]i in both the thorn and the immediately adjacent dendrite. Changes in [Ca2+]i were time locked with the onset of depolarization and the decay began immediately after the termination of depolarization. The peak increase in the Ca2+ signal was significantly greater in the thorns than in the adjacent dendritic shafts. With the use of high-temporal-resolution methods (line scans), differences were also seen in the time course of Ca2+ signals in these two regions. The decay time constants of the Ca2+ signal were faster in thorns than in the adjacent dendritic shafts. These observations suggest that voltage-gated Ca2+ channels are localized directly on the dendritic spines receiving mossy-fiber input. Furthermore, Ca2+ homeostasis within thorny excrescences is distinct from Ca2+ regulation in the dendritic shaft, at least over brief time periods, a finding that could have important implications for synaptic plasticity and signaling.
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Scherf, Thomas, and Frank Angenstein. "Postsynaptic and Spiking Activity of Pyramidal Cells, the Principal Neurons in the Rat Hippocampal CA1 Region, Does Not Control the Resultant BOLD Response: A Combined Electrophysiologic and fMRI Approach." Journal of Cerebral Blood Flow & Metabolism 35, no. 4 (January 7, 2015): 565–75. http://dx.doi.org/10.1038/jcbfm.2014.252.
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The specific role of postsynaptic activity for the generation of a functional magnetic resonance imaging (fMRI) response was determined by a simultaneous measurement of generated field excitatory postsynaptic potentials (fEPSPs) and blood oxygen level-dependent (BOLD) response in the rat hippocampal CA1 region during electrical stimulation of the contralateral CA3 region. The stimulation electrode was placed either in the left CA3a/b or CA3c, causing the preferentially basal or apical dendrites of the pyramidal cells in the right CA1 to be activated. Consecutive stimulations with low-intensity stimulation trains (i.e., 16 pulses for 8 seconds) resulted in clear postsynaptic responses of CA1 pyramidal cells, but in no significant BOLD responses. In contrast, consecutive high-intensity stimulation trains resulted in stronger postsynaptic responses that came along with minor (during stimulation of the left CA3a/b) or substantial (during stimulation of the left CA3c) spiking activity of the CA1 pyramidal cells, and resulted in the generation of significant BOLD responses in the left and right hippocampus. Correlating the electrophysiologic parameters of CA1 pyramidal cell activity (fEPSP and spiking activity) with the resultant BOLD response revealed no positive correlation. Consequently, postsynaptic activity of pyramidal cells, the most abundant neurons in the CA1, is not directly linked to the measured BOLD response.
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Casoli, Tiziana, Giuseppina Di Stefano, Natascia Gracciotti, Simona Giovagnetti, Patrizia Fattoretti, Moreno Solazzi, and Carlo Bertoni–Freddari. "Cellular Distribution of GAP-43 mRNA in Hippocampus and Cerebellum of Adult Rat Brain by In Situ RT-PCR." Journal of Histochemistry & Cytochemistry 49, no. 9 (September 2001): 1195–96. http://dx.doi.org/10.1177/002215540104900917.
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The growth-associated protein GAP-43 is a presynaptic membrane phosphoprotein that plays a key role in guiding the growth of axons and in modulating the formation of new synapses. To identify the cells that synthesize GAP-43 mRNA, we applied direct in situ reverse transcription-polymerase chain reaction (in situ RT-PCR) in cerebellum and hippocampus of adult rat brain. In situ RT-PCR revealed GAP-43 mRNA in cerebellar granule cells, in Purkinje cells and in some interneurons of the molecular layer. Previous in situ hybridization studies had demonstrated a dense label throughout the granular layer of the cerebellar cortex but no labeling of other cerebellar neurons. Hippocampal cells showing distinct GAP-43 mRNA signal after in situ RT-PCR were CA1 and CA3 pyramidal neurons, CA4 hilar cells, and dentate gyrus granule cells, whereas in situ hybridization studies had detected GAP-43 mRNA only in CA3 and CA1 pyramidal neurons. Our data indicate that GAP-43 mRNA is widely distributed, suggesting that many cell types are potentially involved in synaptic plasticity events. (J Histochem Cytochem 49:1195–1196, 2001)
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Christian, E. P., and F. E. Dudek. "Characteristics of local excitatory circuits studied with glutamate microapplication in the CA3 area of rat hippocampal slices." Journal of Neurophysiology 59, no. 1 (January 1, 1988): 90–109. http://dx.doi.org/10.1152/jn.1988.59.1.90.
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1. Local neuronal circuits in CA3 of hippocampal slices were studied by recording excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) intracellularly during glutamate microapplication in CA3. Control experiments validated this approach by providing evidence that glutamate microdrops stimulated neurons but not axons-of-passage or axon terminals in CA3. 2. Glutamate microdrops (10-20 mM, 10-20 microns diam) increased the firing frequency of extracellularly recorded dentate granule cells for 5–10 s when applied to their somata but not when applied to their mossy fiber axons and terminals in the hilus and in CA3. 3. Glutamate microapplications to granule cell somata, but not to mossy fiber axons, also increased the frequency of intracellularly recorded EPSPs in CA3 pyramidal cells for 5-10 s. This provided a second line of evidence that glutamate did not cause firing in mossy fiber axons synapsing in CA3. 4. In slices where the CA3 region was surgically separated from the dentate gyrus and CA2, glutamate microdrops placed in the CA3 stratum pyramidale within 400 microns of intracellularly recorded pyramidal cells increased the frequency of EPSPs and IPSPs. Tetrodotoxin (1 microgram/ml) blocked these increases in PSP frequency, indicating that they did not result from glutamate-induced depolarization and associated transmitter release from presynaptic terminals. Increases in PSP frequency were interpreted to reflect glutamate activations of CA3 neurons with local synaptic connections to recorded cells. 5. Low concentrations of picrotoxin (PTX, 5-10 microM) blocked glutamate-induced increases in IPSP frequency and often revealed increases in EPSP frequency where they were not previously observed. This suggests that recurrent inhibitory circuits normally mask or block transmission through recurrent excitatory pathways in CA3. 6. In five experiments following PTX treatment (7.5–10 microM), large and prolonged (up to 2 min) increases in EPSP frequency were observed in CA3 pyramidal cells to glutamate microapplications in CA3. Rhythmic epileptiform bursts eventually occurred in two of these cases, suggesting that the protracted increases in EPSP frequency represent a form of reverberating excitation during a transition from normal to epileptic states. 7. Sixteen CA3 pyramidal cells were recorded in PTX (5-10 microM) during glutamate microapplications at 200 and 400 microns on each side of the recording site. The most consistent glutamate-induced increases in EPSP frequency occurred to microapplications 200 microns from recording sites on the hilar side.(ABSTRACT TRUNCATED AT 400 WORDS)
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Mody, I., J. D. Lambert, and U. Heinemann. "Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices." Journal of Neurophysiology 57, no. 3 (March 1, 1987): 869–88. http://dx.doi.org/10.1152/jn.1987.57.3.869.
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The effect of low extracellular Mg2+ concentration ([Mg2+]o) on neuronal activity was studied in rat hippocampal slices. After 20–40 min of perfusion with Mg2+-free medium, when [Mg2+]o declined to approximately 0.1–0.4 mM, spontaneous field potentials developed in the CA1 and CA3 regions, but not in the dentate gyrus. In the CA3 pyramidal cell layer, these potentials consisted of repetitive (0.3–0.5 Hz), 40- to 120-ms-long positive deflections (2–5 mV) with superimposed population spikes. In the stratum (str.) pyramidale of the CA1 region, positive-negative deflections (less than 3 mV) lasting for 30–80 ms were observed, which occurred with a frequency of 0.3-0.5 Hz. In some cases, longer lasting and rapidly recurring events were also observed. In CA3 pyramidal cells, the intracellular correlates of the field potential transients were 20- to 30-mV paroxysmal depolarization shifts (PDS) with superimposed bursts of action potentials, followed by large (greater than 10 mV), 500- to 1,200-ms-long afterhyperpolarizations (AHP). In contrast, pyramidal neurons of the CA1 area did not show PDSs; instead, sequences of excitatory postsynaptic potentials (EPSPs)/inhibitory postsynaptic potentials (IPSPs) accompanied the transient field potential changes. Occasionally, spontaneous EPSPs/IPSPs, occurring with high frequencies, could also be observed in CA1 without any field potential transients. In both hippocampal regions, the epileptiform activity evolved without significant alterations in the resting membrane potential (RMP) and input resistance (RN) of the neurons, although a 2- to 5-mV reduction in action potential threshold was noted. The spontaneous activity in Mg2+-free medium was readily suppressed by raising the extracellular Ca2+ concentration ([Ca2+]o) from 1.6 to 3.6 mM. The perfusion of 10-30 microns DL-2-amino-5-phosphonovaleric acid (2-APV), an antagonist for the glutamate receptors of the N-methyl-D-aspartate (NMDA) type, also attenuated or reversibly blocked the spontaneous activity. Surgical isolation of area CA1 from CA3 ceased the occurrence of the transients in CA1 but not in CA3. The synaptic input/output curves were shifted to the left in the absence of [Mg2+]o. Threshold intensity for eliciting population spikes was 50-75% of that in normal medium. Paired-pulse facilitation was still present near threshold, but was reduced at higher stimulus intensities. Decreases in [Ca2+]o, produced by repetitive stimulation (20-Hz/5-10 s) of the Schaffer collateral/commissural pathway and monitored with ion-selective microelectrodes in the CA1 region, were enhanced in Mg2+-free medium.(ABSTRACT TRUNCATED AT 400 WORDS)
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Traub, R. D., R. K. Wong, R. Miles, and H. Michelson. "A model of a CA3 hippocampal pyramidal neuron incorporating voltage-clamp data on intrinsic conductances." Journal of Neurophysiology 66, no. 2 (August 1, 1991): 635–50. http://dx.doi.org/10.1152/jn.1991.66.2.635.
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1. We have developed a 19-compartment cable model of a guinea pig CA3 pyramidal neuron. Each compartment is allowed to contain six active ionic conductances: gNa, gCa, gK(DR) (where DR stands for delayed rectifier), gK(A), gK(AHP), and gK(C). THe conductance gCa is of the high-voltage activated type. The model kinetics for the first five of these conductances incorporate voltage-clamp data obtained from isolated hippocampal pyramidal neurons. The kinetics of gK(C) are based on data from bullfrog sympathetic neurons. The time constant for decay of submembrane calcium derives from optical imaging of Ca signals in Purkinje cell dendrites. 2. To construct the model from available voltage-clamp data, we first reproduced current-clamp records from a model isolated neuron (soma plus proximal dendrites). We next assumed that ionic channel kinetics in the dendrites were the same as in the soma. In accord with dendritic recordings and calcium-imaging data, we also assumed that significant gCa occurs in dendrites. We then attached sections of basilar and apical dendritic cable. By trial and error, we found a distribution (not necessarily unique) of ionic conductance densities that was consistent with current-clamp records from the soma and dendrites of whole neurons and from isolated apical dendrites. 3. The resulting model reproduces the Ca(2+)-dependent spike depolarizing afterpotential (DAP) recorded after a stimulus subthreshold for burst elicitation. 4. The model also reproduces the behavior of CA3 pyramidal neurons injected with increasing somatic depolarizing currents: low-frequency (0.3-1.0 Hz) rhythmic bursting for small currents, with burst frequency increasing with current magnitude; then more irregular bursts followed by afterhyperpolarizations (AHPs) interspersed with brief bursts without AHPs; and finally, rhythmic action potentials without bursts. 5. The model predicts the existence of still another firing pattern during tonic depolarizing dendritic stimulation: brief bursts at less than 1 to approximately 12 Hz, a pattern not observed during somatic stimulation. These bursts correspond to rhythmic dendritic calcium spikes. 6. The model CA3 pyramidal neuron can be made to resemble functionally a CA1 pyramidal neuron by increasing gK(DR) and decreasing dendritic gCa and gK(C). Specifically, after these alterations, tonic depolarization of the soma leads to adapting repetitive firing, whereas stimulation of the distal dendrites leads to bursting. 7. A critical set of parameters concerns the regulation of the pool of intracellular [Ca2+] that interacts with membrane channels (gK(C) and gK(AHP)), particularly in the dendrites.(ABSTRACT TRUNCATED AT 400 WORDS)
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MacVicar, Brian A., and Henrik Jahnsen. "Uncoupling of CA3 pyramidal neurons by propionate." Brain Research 330, no. 1 (March 1985): 141–45. http://dx.doi.org/10.1016/0006-8993(85)90015-0.
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Stepanov, A. S., V. A. Akulinin, S. S. Stepanov, D. B. Avdeev, and A. V. Gorbunova. "Neurons Communication in the Hippocampus of Field CA3 of the White Rat Brain after Acute ischemia." General Reanimatology 14, no. 5 (October 28, 2018): 38–49. http://dx.doi.org/10.15360/1813-9779-2018-5-38-49.
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The aim of this studywas to compare the pyramidal neurons, their processes and synapses in the stratum lucidum, stratum radiatum and stratum lacunosum of the molecular layer of the field CA3 of the hippocampus of the brain of white rats in the normal state and after acute ischemia caused by a 20-minute occlusion of the common carotid arteries.Materials and methods.In the experiment, using histological methods (hematoxylin and eosin, staining by Nissle and immunohistochemistry for p38, MAP-2) and electron microscopy, the pyramidal neurons of field CA3, their processes and synapses in stratum lucidum, stratum radiatum and stratum lacunosum of the molecular layer were studied. The main group included animals in the reperfusion period (1, 3, 7, 14, 21, and 30 days;n=30), comparison group — falsely operated animals (n=20). Morphometric analysis was performed using ImageJ 1.46, the verification of statistical hypotheses — Statistica 8.0.Results.After occlusion of the common carotid arteries (CCAO) in the field CA3 of hippocampus, reactive, compensatory and reparative reorganization of pyramidal neurons and their communication structures was noted. On day 1, there was a decrease, and then (days 3—14) restoration of the total number of synapses and of P38-positive material within the area of synapses. According to electron microscopy, in the early post-ischemic period, the total numerical density of synaptic contacts in the stratum lacunosum of the molecular layer decreased by 44.8%, and after 14 days recovered to control. In stratum lucidum, the area of P38-positive material decreased by 8.8% after 1 day, and recovered after 3—7 days.Conclusion.After the CCAO, the communication systems of the pyramid neurons of the field CA3 hippocampus of white rats were reorganized. Neurons of the field CA3 had high tolerance to ischemia and ability to restore interneural relations after reperfusion. In the surviving neurons, high levels of the cytoskeleton (MAP-2) marker and synaptic vesicles (p38) were detected. Data demonstrate structural and functional safety of all components of the communication system of a significant part of pyramidal neurons in acute ischemia. After reperfusion, the most significant alterations included the reconstructed interneuron synapses in the stratum radiatum and the lacunosum molecular layer.
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Sá, Maria José, Carlos Ruela, and Maria Dulce Madeira. "Dendritic right/left asymmetries in the neurons of the human hippocampal formation: a quantitative Golgi study." Arquivos de Neuro-Psiquiatria 65, no. 4b (December 2007): 1105–13. http://dx.doi.org/10.1590/s0004-282x2007000700003.
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OBJECTIVE: To search for right/left asymmetries in the dendritic trees of the neuronal populations and in the cell-free layer volumes of the human hipoccampal formation. METHOD: In necropsic material obtained from six male individuals we performed a quantitative Golgi study of the dendritic trees of dentate granules, CA3 and CA1 pyramidal neurons and a volumetric analysis of dentate gyrus molecular layer, strata oriens plus alveus and strata lacunosum-moleculare plus radiatum of CA3 and CA1 fields. RESULTS: We found inter-hemispheric asymmetries in the dendrites trees of all neurons, reaching the significant level in the number of granule cells dendritic segments (higher in the left than in the right hemisphere), dendritic branching density of CA3 pyramidal cells and mean dendritic length of CA1 apical terminal segments (higher in the right than in the opposite side). No volumetric differences were observed. CONCLUSION: This study points to different anatomical patterns of connectivity in the hippocampal formations of both hemispheres which may underlie functional asymmetries.
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Cornell-Bell, A. H., P. G. Thomas, and J. M. Caffrey. "Ca2+ and filopodial responses to glutamate in cultured astrocytes and neurons." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S206—S218. http://dx.doi.org/10.1139/y92-264.
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Neurons and glia exhibit complex homeostatic interactions via shared extracellular space which can involve metabolites, inorganic ions, and neurotransmitters. Focal application of glutamate to both human and rat central nervous system astrocytes in primary culture produced a rapid, transient increase in both cytoplasmic and nuclear Ca2+. These Ca2+ waves can propagate at up to 15–20 μm/s for long distances (millimetres) through the astrocyte syncitium. Oscillatory Ca2+ signals were frequently observed under control conditions and were enhanced by glutamate application. These Ca2+ signals were paralleled by rapid extensions of filopodia from the astrocyte cell margin and apical surface near the point of glutamate application. Focal application of glutamate to rat hippocampal neurons also elicited rapid, transient increases in intracellular Ca2+. Levels of Ca2+ signals were consistently two- to three-fold greater in pyramidal neurons cultured from CA1 than in those from CA3. Filopodial extension was extensive in CA1 neurons, but rare in CA3 neurons, and in either case observable only during the first few days of primary culture. Diversity of glial and neuronal responses to binding the glutamate receptors may reflect their roles in homeostatic interactions.Key words: glutamate, astrocytes, hippocampal neurons, Ca2+ signals, filopodia.
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Fisher, R., and D. Johnston. "Differential modulation of single voltage-gated calcium channels by cholinergic and adrenergic agonists in adult hippocampal neurons." Journal of Neurophysiology 64, no. 4 (October 1, 1990): 1291–302. http://dx.doi.org/10.1152/jn.1990.64.4.1291.
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1. Pharmacologic agents known to modulate long-term potentiation (LTP) at the mossy fiber-to-CA3 pyramidal neuron synapse were tested for their effects on the activity of single voltage-gated calcium channels in adult CA3 pyramidal neurons. 2. Single-channel current recordings of three types of voltage-gated calcium channels were made from acutely exposed CA3 pyramidal neurons of the adult guinea pig hippocampus. 3. The beta-adrenergic agonist isoproterenol (10 microM), which is known to enhance LTP, increased the activity of the two high-threshold calcium channels (N and L) with no striking effect on the low-threshold (T) channel. 4. The muscarinic agonists carbachol and muscarine (1-10 microM), the latter of which has been shown to inhibit LTP, decreased the probability of opening of L channels, increased the probability of opening of T channels, and had no effect on N channels. The effects were blocked by 0.1 microM atropine. 5. These results are consistent with the hypothesis that neuromodulation of mossy fiber LTP occurs, at least in part, through the modulation of postsynaptic, voltage-gated calcium channels.
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Braun, Wilhelm, and Raoul-Martin Memmesheimer. "High-frequency oscillations and sequence generation in two-population models of hippocampal region CA1." PLOS Computational Biology 18, no. 2 (February 17, 2022): e1009891. http://dx.doi.org/10.1371/journal.pcbi.1009891.
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Hippocampal sharp wave/ripple oscillations are a prominent pattern of collective activity, which consists of a strong overall increase of activity with superimposed (140 − 200 Hz) ripple oscillations. Despite its prominence and its experimentally demonstrated importance for memory consolidation, the mechanisms underlying its generation are to date not understood. Several models assume that recurrent networks of inhibitory cells alone can explain the generation and main characteristics of the ripple oscillations. Recent experiments, however, indicate that in addition to inhibitory basket cells, the pattern requires in vivo the activity of the local population of excitatory pyramidal cells. Here, we study a model for networks in the hippocampal region CA1 incorporating such a local excitatory population of pyramidal neurons. We start by investigating its ability to generate ripple oscillations using extensive simulations. Using biologically plausible parameters, we find that short pulses of external excitation triggering excitatory cell spiking are required for sharp/wave ripple generation with oscillation patterns similar to in vivo observations. Our model has plausible values for single neuron, synapse and connectivity parameters, random connectivity and no strong feedforward drive to the inhibitory population. Specifically, whereas temporally broad excitation can lead to high-frequency oscillations in the ripple range, sparse pyramidal cell activity is only obtained with pulse-like external CA3 excitation. Further simulations indicate that such short pulses could originate from dendritic spikes in the apical or basal dendrites of CA1 pyramidal cells, which are triggered by coincident spike arrivals from hippocampal region CA3. Finally we show that replay of sequences by pyramidal neurons and ripple oscillations can arise intrinsically in CA1 due to structured connectivity that gives rise to alternating excitatory pulse and inhibitory gap coding; the latter denotes phases of silence in specific basket cell groups, which induce selective disinhibition of groups of pyramidal neurons. This general mechanism for sequence generation leads to sparse pyramidal cell and dense basket cell spiking, does not rely on synfire chain-like feedforward excitation and may be relevant for other brain regions as well.
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de Sevilla, David Fernández, Julieta Garduño, Emilio Galván, and Washington Buño. "Calcium-Activated Afterhyperpolarizations Regulate Synchronization and Timing of Epileptiform Bursts in Hippocampal CA3 Pyramidal Neurons." Journal of Neurophysiology 96, no. 6 (December 2006): 3028–41. http://dx.doi.org/10.1152/jn.00434.2006.
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Calcium-activated potassium conductances regulate neuronal excitability, but their role in epileptogenesis remains elusive. We investigated in rat CA3 pyramidal neurons the contribution of the Ca2+-activated K+-mediated afterhyperpolarizations (AHPs) in the genesis and regulation of epileptiform activity induced in vitro by 4-aminopyridine (4-AP) in Mg2+-free Ringer. Recurring spike bursts terminated by prolonged AHPs were generated. Burst synchronization between CA3 pyramidal neurons in paired recordings typified this interictal-like activity. A downregulation of the medium afterhyperpolarization (mAHP) paralleled the emergence of the interictal-like activity. When the mAHP was reduced or enhanced by apamin and EBIO bursts induced by 4-AP were increased or blocked, respectively. Inhibition of the slow afterhyperpolarization (sAHP) with carbachol, t-ACPD, or isoproterenol increased bursting frequency and disrupted burst regularity and synchronization between pyramidal neuron pairs. In contrast, enhancing the sAHP by intracellular dialysis with KMeSO4 reduced burst frequency. Block of GABAA–B inhibitions did not modify the abnormal activity. We describe novel cellular mechanisms where 1) the inhibition of the mAHP plays an essential role in the genesis and regulation of the bursting activity by reducing negative feedback, 2) the sAHP sets the interburst interval by decreasing excitability, and 3) bursting was synchronized by excitatory synaptic interactions that increased in advance and during bursts and decreased throughout the subsequent sAHP. These cellular mechanisms are active in the CA3 region, where epileptiform activity is initiated, and cooperatively regulate the timing of the synchronized rhythmic interictal-like network activity.
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Lee, Tae-Kyeong, Myoung Cheol Shin, Ji Hyeon Ahn, Dae Won Kim, Bora Kim, Hyejin Sim, Jae-Chul Lee, et al. "CD200 Change Is Involved in Neuronal Death in Gerbil Hippocampal CA1 Field Following Transient Forebrain Ischemia and Postischemic Treatment with Risperidone Displays Neuroprotection without CD200 Change." International Journal of Molecular Sciences 22, no. 3 (January 23, 2021): 1116. http://dx.doi.org/10.3390/ijms22031116.
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It has been reported that CD200 (Cluster of Differentiation 200), expressed in neurons, regulates microglial activation in the central nervous system, and a decrease in CD200 expression causes an increase in microglial activation and neuronal loss. The aim of this study was to investigate time-dependent changes in CD200 expression in the hippocampus proper (CA1, 2, and 3 fields) after transient forebrain ischemia for 5 min in gerbils. In this study, 5-min ischemia evoked neuronal death (loss) of pyramidal neurons in the CA1 field, but not in the CA2/3 fields, at 5 days postischemia. In the sham group, CD200 expression was found in pyramidal neurons of the CA1 field, and the immunoreactivity in the group with ischemia was decreased at 6 h postischemia, dramatically increased at 12 h postischemia, decreased (to level found at 6 h postischemia) at 1 and 2 days postischemia, and significantly increased again at 5 days postischemia. At 5 days postischemia, CD200 immunoreactivity was strongly expressed in microglia and GABAergic neurons. However, in the CA3 field, the change in CD200 immunoreactivity in pyramidal neurons was markedly weaker than that in the CA1 field, showing there was no expression of CD 200 in microglia and GABAergic neurons. In addition, treatment of 10 mg/kg risperidone (an atypical antipsychotic drug) after the ischemia hardly changed CD200 immunoreactivity in the CA1 field, showing that CA1 pyramidal neurons were protected from the ischemic injury. These results indicate that the transient ischemia-induced change in CD200 expression may be associated with specific and selective neuronal death in the hippocampal CA1 field following transient forebrain ischemia.
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Tanabe, Mitsuo, Masahiro Mori, Beat H. Gähwiler, and Urs Gerber. "Apamin-Sensitive Conductance Mediates the K+ Current Response During Chemical Ischemia in CA3 Pyramidal Cells." Journal of Neurophysiology 82, no. 6 (December 1, 1999): 2876–82. http://dx.doi.org/10.1152/jn.1999.82.6.2876.
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Pyramidal cells typically respond to ischemia with initial transient hyperpolarization, which may represent a neuroprotective response. To identify the conductance underlying this hyperpolarization in CA3 pyramidal neurons of rat hippocampal organotypic slice cultures, recordings were obtained using the single-electrode voltage-clamp technique. Brief chemical ischemia (2 mM 2-deoxyglucose and 3 mM NaN3, for 4 min) induced a response mediated by an increase in K+ conductance. This current was blocked by intracellular application of the Ca2+ chelator, bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA), reduced with low external [Ca2+], and inhibited by a selective L-type Ca2+ channel inhibitor, isradipine, consistent with the activation of a Ca2+-dependent K+ conductance. Experiments with charybdotoxin (10 nM) and tetraethylammonium (TEA; 1 mM), or with the protein kinase C activator, phorbol 12,13-diacetate (PDAc; 3 μM), ruled out an involvement of a large conductance–type or an apamin-insensitive small conductance, respectively. In the presence of apamin (1 μM), however, the outward current was significantly reduced. These results demonstrate that in rat hippocampal CA3 pyramidal neurons an apamin-sensitive Ca2+-dependent K+ conductance is activated in response to brief ischemia generating a pronounced outward current.
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Banerjee, Jyotirmoy, Manickavasagom Alkondon, Edson X. Albuquerque, and Edna F. R. Pereira. "Contribution of CA3 and CA1 pyramidal neurons to the tonic α7 nAChR-dependent glutamatergic input to CA1 pyramidal neurons." Neuroscience Letters 554 (October 2013): 167–71. http://dx.doi.org/10.1016/j.neulet.2013.08.025.
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Yokota, Masayuki, Takaomi C. Saido, Eiichi Tani, Ikuya Yamaura, and Nobutaka Minami. "Cytotoxic Fragment of Amyloid Precursor Protein Accumulates in Hippocampus after Global Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 16, no. 6 (November 1996): 1219–23. http://dx.doi.org/10.1097/00004647-199611000-00016.
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We developed an antibody specific to β-amyloid precursor protein (βAPP) fragments possessing the exact amino terminus of the β-amyloid peptide and examined its induction in postischemic hippocampus. In control hippocampus, this APP fragment was lightly observed in pyramidal neurons of CA sectors and dentate granule cells. Transient forebrain ischemia enhanced accumulation of the APP fragment in CA1 pyramidal neurons. Seven days after the ischemia, while the APP fragment was still observed in dentate granule cells and CA3 neurons, it disappeared in dead CA1 neurons. While astrocytes did not show in any immunoreactivity throughout the experiment, those in the CA1 sector showed moderate immunoreactivity 7 days after the ischemia. The APP fragment has a cytotoxic effect on cultured neurons. These results suggest that the accumulation of the cytotoxic APP fragment in CA1 neurons may play a role in the development of delayed neuronal death after the ischemic insult.
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Makara, Judit K., and Jeffrey C. Magee. "Variable Dendritic Integration in Hippocampal CA3 Pyramidal Neurons." Neuron 80, no. 6 (December 2013): 1438–50. http://dx.doi.org/10.1016/j.neuron.2013.10.033.
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McEwen, Bruce S. "Stress-induced remodeling of hippocampal CA3 pyramidal neurons." Brain Research 1645 (August 2016): 50–54. http://dx.doi.org/10.1016/j.brainres.2015.12.043.
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Łuszczewska-Sierakowska, Iwona, Agata Wawrzyniak, Marcin R. Tatara, Anna Charuta, Jacek Baj, and Ryszard Maciejewski. "Morphometric characteristics of neurons in the hippocampal CA1-CA4 fields of the American." Medycyna Weterynaryjna 72, no. 11 (2016): 704–8. http://dx.doi.org/10.21521/mw.5584.
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The aim of the study was a quantitative and cytoarchitectonic examination of neurons of the ventral hippocampal CA1-CA4 fields in somatically mature female American mink (Neovison vison) (N = 6). Brains were removed and examined under a light microscope. The samples were stained by Nissl’s standard method, and histological samples were used for morphometric analysis. All ventral hippocampal CA1-CA4 fields were analyzed cytoarchitectonically and morphometrically with a calibrated image analysis system that consisted of a computer equipped with the Cell^D software Soft Imaging System (SIS) with an integrated digital camera Colorview IIIu (Soft Imaging System). Morphometric investigations of the pyramidal layer showed that the cells of the hippocampal CA1-CA4 fields in adult female American mink differ in size, shape, cell area, nucleus area and the nucleus-to-cell ratio (in %). The cells of the CA2 field were densely arranged, pyramidal and contained a small amount of cytoplasm; their size was differentiated. They were the largest in size (15.06 μm) and diameter (14.5 μm). The cells of the CA1 field had the smallest size (8.5 μm) and diameter (8.6 μm). In the CA3 field, small, densely packed neurons dominated, whereas neurons in the CA4 field formed a thin strand of loosely arranged cells. Given the increasing interest in hippocampal areas, it is necessary to continue studies of their morphology and morphometry in healthy animals and in those suffering from neurodegenerative diseases.
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Buss, Eric W., Nicola J. Corbett, Joshua G. Roberts, Natividad Ybarra, Timothy F. Musial, Dina Simkin, Elizabeth Molina-Campos, et al. "Cognitive aging is associated with redistribution of synaptic weights in the hippocampus." Proceedings of the National Academy of Sciences 118, no. 8 (February 16, 2021): e1921481118. http://dx.doi.org/10.1073/pnas.1921481118.
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Behaviors that rely on the hippocampus are particularly susceptible to chronological aging, with many aged animals (including humans) maintaining cognition at a young adult-like level, but many others the same age showing marked impairments. It is unclear whether the ability to maintain cognition over time is attributable to brain maintenance, sufficient cognitive reserve, compensatory changes in network function, or some combination thereof. While network dysfunction within the hippocampal circuit of aged, learning-impaired animals is well-documented, its neurobiological substrates remain elusive. Here we show that the synaptic architecture of hippocampal regions CA1 and CA3 is maintained in a young adult-like state in aged rats that performed comparably to their young adult counterparts in both trace eyeblink conditioning and Morris water maze learning. In contrast, among learning-impaired, but equally aged rats, we found that a redistribution of synaptic weights amplifies the influence of autoassociational connections among CA3 pyramidal neurons, yet reduces the synaptic input onto these same neurons from the dentate gyrus. Notably, synapses within hippocampal region CA1 showed no group differences regardless of cognitive ability. Taking the data together, we find the imbalanced synaptic weights within hippocampal CA3 provide a substrate that can explain the abnormal firing characteristics of both CA3 and CA1 pyramidal neurons in aged, learning-impaired rats. Furthermore, our work provides some clarity with regard to how some animals cognitively age successfully, while others’ lifespans outlast their “mindspans.”
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Azimi-Zonooz, Aryan, C. William Shuttleworth, and John A. Connor. "GABAergic Protection of Hippocampal Pyramidal Neurons Against Glutamate Insult: Deficit in Young Animals Compared to Adults." Journal of Neurophysiology 96, no. 1 (July 2006): 299–308. http://dx.doi.org/10.1152/jn.01082.2005.
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Hypoxia-ischemia (HI) injury in neonatal animals leads to selective regional loss of neurons including CA1 and CA3 pyramidal neurons of the hippocampus as well as nonlethal pathologies. Glutamate-receptor over-activation and Ca2+ influx are involved in these neonatal changes. We examined glutamate-evoked Ca2+ responses in neonatal (PN 7–13) and young adult (PN 21–27) CA1 pyramidal neurons in acute slices from rats. In neonates, transient exposure to glutamate produced large Ca2+ increases throughout neurons, including distal dendrites (primary Ca2+ responses). Repeated exposures resulted in sustained Ca2+ increases in apical dendrites (secondary Ca2+ responses) that were independent of continued glutamate exposure. These responses propagated and invaded the soma, resulting in irrecoverably high Ca2+ elevations. In neurons from adults, identical glutamate exposure evoked primary Ca2+ responses only in somata and proximal apical dendrites. Repeated glutamate exposures in the adult neurons also led to secondary Ca2+ responses, but they arose in the peri-somatic region and then spread outward to distal apical dendrites, again without recovery. More stimuli were required to initiate secondary responses in neurons from adult versus neonates. Block of GABAA receptors in adults caused the primary and secondary responses to revert to the spatial pattern seen in the neonates and greatly increased their vulnerability to glutamate. These findings suggest that neurodegenerative secondary Ca2+ events may be important determinants of susceptibility to HI injury in the developing CNS and that immature CA1 neurons may be more susceptible to excitotoxic injury due at least in part to insufficient development of GABAergic inputs to their dendrites.
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Akdogan, Ilgaz, Nedim Unal, and Esat Adiguzel. "ESTIMATION OF THE NUMBER OF NEURONS IN THE HIPPOCAMPUS OF RATS WITH PENICILLIN INDUCED EPILEPSY." Image Analysis & Stereology 21, no. 2 (May 3, 2011): 117. http://dx.doi.org/10.5566/ias.v21.p117-120.
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Epilepsy is a neurological disease arising from strong and uncontrollable electrical firings of a group of neurons in the central nervous system. Experimental epileptic models have been developed to assess the physiopathology of epileptic seizures. This study was undertaken to estimate the number of neurons in the rat hippocampus with penicillin induced epilepsy, using a stereological method, "the optical fractionator". In the experimental group, 500 IU penicillin-G was injected intra-cortically, and in the control group, the same volume of saline was administered. A week later, the animals were decapitated and their brains were removed by craniatomy. Frozen brains were cut with a thickness of 150 ěm in a cryostat. Sections were collected by systematic random sampling and stained with hematoxylen-eosin. Microscopic images of pyramidal cell layers from hippocampus CA1, CA2 and CA3 subfields were then transferred to a monitor, using a 100x objective (N.A. = 1.25). Using the optical disector method, the neurons were counted in the frames and determined with a fractionator sampling scheme. The total pyramidal neuron number was then estimated using the optical fractionator method. The total pyramidal neuron number was found to be statistically lower in the experimental group (mean = 142,888 ± 11,745) than in the control group (mean = 177,953 ± 10,907) (p < 0.05). The results suggest that a decrease in the hippocampal neuronal number in a penicillin model of epilepsy can be determined objectively and efficiently using the optical fractionator method.
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Lana, Daniele, Elisabetta Gerace, Giada Magni, Francesca Cialdai, Monica Monici, Guido Mannaioni, and Maria Grazia Giovannini. "Hypoxia/Ischemia-Induced Rod Microglia Phenotype in CA1 Hippocampal Slices." International Journal of Molecular Sciences 23, no. 3 (January 26, 2022): 1422. http://dx.doi.org/10.3390/ijms23031422.
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The complexity of microglia phenotypes and their related functions compels the continuous study of microglia in diseases animal models. We demonstrated that oxygen-glucose deprivation (OGD) induced rapid, time- and space-dependent phenotypic microglia modifications in CA1 stratum pyramidalis (SP) and stratum radiatum (SR) of rat organotypic hippocampal slices as well as the degeneration of pyramidal neurons, especially in the outer layer of SP. Twenty-four h following OGD, many rod microglia formed trains of elongated cells spanning from the SR throughout the CA1, reaching the SP outer layer where they acquired a round-shaped amoeboid phagocytic head and phagocytosed most of the pyknotic, damaged neurons. NIR-laser treatment, known to preserve neuronal viability after OGD, prevented rod microglia formation. In CA3 SP, pyramidal neurons were less damaged, no rod microglia were found. Thirty-six h after OGD, neuronal damage was more pronounced in SP outer and inner layers of CA1, rod microglia cells were no longer detectable, and most microglia were amoeboid/phagocytic. Damaged neurons, more numerous 36 h after OGD, were phagocytosed by amoeboid microglia in both inner and outer layers of CA1. In response to OGD, microglia can acquire different morphofunctional phenotypes which depend on the time after the insult and on the subregion where microglia are located.
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Mori, Masahiro, Beat H. Gähwiler, and Urs Gerber. "Recruitment of an inhibitory hippocampal network after bursting in a single granule cell." Proceedings of the National Academy of Sciences 104, no. 18 (April 16, 2007): 7640–45. http://dx.doi.org/10.1073/pnas.0702164104.
Full textAbstract:
The hippocampal CA3 area, an associational network implicated in memory function, receives monosynaptic excitatory as well as disynaptic inhibitory input through the mossy-fiber axons of the dentate granule cells. Synapses made by mossy fibers exhibit low release probability, resulting in high failure rates at resting discharge frequencies of 0.1 Hz. In recordings from functionally connected pairs of neurons, burst firing of a granule cell increased the probability of glutamate release onto both CA3 pyramidal cells and inhibitory interneurons, such that subsequent low-frequency stimulation evoked biphasic excitatory/inhibitory responses in a CA3 pyramidal cell, an effect lasting for minutes. Analysis of the unitary connections in the circuit revealed that granule cell bursting caused powerful activation of an inhibitory network, thereby transiently suppressing excitatory input to CA3 pyramidal cells. This phenomenon reflects the high incidence of spike-to-spike transmission at granule cell to interneuron synapses, the numerically much greater targeting by mossy fibers of inhibitory interneurons versus principal cells, and the extensively divergent output of interneurons targeting CA3 pyramidal cells. Thus, mossy-fiber input to CA3 pyramidal cells appears to function in three distinct modes: a resting mode, in which synaptic transmission is ineffectual because of high failure rates; a bursting mode, in which excitation predominates; and a postbursting mode, in which inhibitory input to the CA3 pyramidal cells is greatly enhanced. A mechanism allowing the transient recruitment of inhibitory input may be important for controlling network activity in the highly interconnected CA3 pyramidal cell region.
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Pangestiningsih, Tri Wahyu, Ariana Ariana, Irma Padeta, Arvendi Rahma Jadi, and Woro Danur Wendo. "Distribusi neuron serotonergik pada hipokampus Lasiwen (Myotis sp) sebagai satwa liar yang berpotensi menjadi reservoir virus rabies." Jurnal Sain Veteriner 37, no. 1 (August 5, 2019): 97. http://dx.doi.org/10.22146/jsv.42914.
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Myotis sp is an Indonesian microchiropteran, insectivore bat that potential to be a reservoir for rabies virus. Rabies is fatal viral encephalitis and bat could act as wildlife potential reservoirs for the rabies virus and can transmit the disease to humans as the zoonotic disease. Hippocampus is one of diagnostic tissue for rabies disease and serotonergic neuron could involved in pathogenesis of rabies disease. The aim of the study is to investigate the distribution of serotonergic neurons in Myotis sp hippocampus. Five Myotis sp. were captured from wild population in Central Java, and were humanly anesthetized using ketamine and xylazin. The animals were perfused intracardially using NaCl 0.9% as the pre-rinse followed by 10% formaldehyde to fix it. The cerebrums were collected and processing the for paraffin embedding. Cerebrums were sectioning in saggital sections, 12 µm thickness serially with 120 µm intervals. The tissues were staining immunohistochemistry using antibody to serotonin (1/300; Bioss, Cat. No: bs-1126R) 2 night incubation in 4 oC temperature. The solution for blocking background, secondary antibody, avidin-biotin-peroxidae complex and chromogen using kit Starr Trek Universal HRP Detection System (Biocare Medical, Cat No: STUHRP700) and were analyzed descriptivelly. The results show that serotonergic neuros were distributed in the all area of the of Myotis sp hippocampus. In dentate gyrus neuron serotonergic (Sert-IR)s are round in shape and mostly distributed in the middle layer, few in the superficially also deeper layers. In the hippocampus , the Sert-IR neurons are pyramidal in shape and distributed in the CA1, Ca2 and CA3 areas. In subiculum, the Sert-IR neurons are pyramidal in shape, more wider distributed than in the CA1 with no differences between outer layer and deeper layer. The conclutions of this research are the serotonergic neurons are distributed in the all area of hippocampus
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McBain, C., and R. Dingledine. "Dual-component miniature excitatory synaptic currents in rat hippocampal CA3 pyramidal neurons." Journal of Neurophysiology 68, no. 1 (July 1, 1992): 16–27. http://dx.doi.org/10.1152/jn.1992.68.1.16.
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1. Spontaneous miniature synaptic events were studied with tight-seal whole-cell recordings from CA3 neurons maintained in the hippocampal slice from immature rats (3-15 days). CA3 neurons suffer a constant, high-frequency barrage of inhibitory synaptic input. When inhibitory postsynaptic currents were suppressed by bicuculline, a smaller contribution from excitatory synapses was revealed. 2. Addition of tetrodotoxin (TTX) removed a persistent inward current and substantially reduced the baseline noise facilitating the detection of ,miniature- excitatory currents. Addition of hyperosmotic media increased the frequency of spontaneous excitatory postsynaptic currents (EPSCs). 3. Under both physiological and elevated potassium conditions, individual spontaneous miniature EPSCs (10-30 pA amplitude) were composed of components mediated by N-methyl-D-aspartate (NMDA) and non-NMDA receptors as determined by their voltage dependence, time course, and sensitivity to selective antagonists. 6-Cyano-7-nitro-quinoxaline-2,3-dione (CNQX) or D-2-amino-5-phosphonovaleric acid (D-APV) shifted the amplitude distribution of miniature EPSCs to a smaller mode at both +40 mV and -40 mV. Similar to EPSCs recorded in CA1 neurons, the rise and decay times of the NMDA receptor component were slower than those of the non-NMDA component. The time course of the non-NMDA component was voltage independent. 4. In 13 of 21 neurons, no correlation existed between individual EPSC rise times and their corresponding halfwidth, peak amplitude, or decay time constant. This suggests that the large range of EPSC kinetics observed in each individual neuron was not due solely to cable attenuation of EPSCs widely distributed over the dendritic tree. Plots of the mean EPSC rise time against mean halfwidth for each cell, however, revealed a striking correlation, suggesting that in neonates, active synapses may be grouped in a restricted region of the dendritic tree and as such are subject to similar amounts of dendritic filtering. 5. The electrotonic length of CA3 neurons (L = 0.52) predicted that at this maturity the electrotonic compactness of the neuron facilitated voltage control over all but the most distal synapses. The reversal potential of the fast component of spontaneous events was close to 0 mV, whereas the reversal potential of exogenously applied kainate and NMDA was more positive. This discrepancy likely reflects a compromise of the voltage clamp by the activation of conductances distributed over the entire cell.(ABSTRACT TRUNCATED AT 400 WORDS)
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Fujita, Hiroko, Kohji Sato, Tong-Chun Wen, Yi Peng, and Masahiro Sakanaka. "Differential Expressions of Glycine Transporter 1 and Three Glutamate Transporter mRNA in the Hippocampus of Gerbils with Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 19, no. 6 (June 1999): 604–15. http://dx.doi.org/10.1097/00004647-199906000-00003.
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The extracellular concentrations of glutamate and its co-agonist for the N-methyl-d-aspartate (NMDA) receptor, glycine, may be under the control of amino acid transporters in the ischemic brain, However, there is little information on changes in glycine and glutamate transporters in the hippocampal CA1 field of gerbils with transient forebrain ischemia. This study investigated the spatial and temporal expressions of glycine transporter 1 (GLYT 1) and three glutamate transporter (excitatory amino acid carrier 1, EAAC 1; glutamate/aspartate transporter, GLAST; glutamate transporter 1, GLT1) mRNA in the gerbil hippocampus after 3 minutes of ischemia. The GLYT1 mRNA was transiently upregulated by the second day after ischemia in astrocytelike cells in close vicinity to hippocampal CA1 pyramidal neurons, possibly to reduce glycine concentration in the local extracellular spaces. The EAAC1 mRNA was abundantly expressed in almost all pyramidal neurons and dentate granule cells in the control gerbil hippocampus, whereas the expression level in CA1 pyramidal neurons started to decrease by the fourth day after ischemia in synchrony with degeneration of the CA1 neurons. The GLAST and GLT1 mRNA were rather intensely expressed in the dentate gyrus and CA3 field of the control hippocampus, respectively, but they were weakly expressed in the CA1 field before and after ischemia. As GLAST and GLT1 play a major role in the control of extracellular glutamate concentration, the paucity of these transporters in the CA1 field may account for the vulnerability of CA1 neurons to ischemia, provided that the functional GLAST and GLT1 proteins are also less in the CA1 field than in the CA3 field. This study suggests that the amino acid transporters play pivotal roles in the process of delayed neuronal death in the hippocampal CA1 field.
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Nasrallah, Kaoutsar, Rebecca A. Piskorowski, and Vivien Chevaleyre. "Inhibitory Plasticity Permits the Recruitment of CA2 Pyramidal Neurons by CA3." eneuro 2, no. 4 (July 2015): ENEURO.0049–15.2015. http://dx.doi.org/10.1523/eneuro.0049-15.2015.
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Muller, W., and U. Misgeld. "Inhibitory role of dentate hilus neurons in guinea pig hippocampal slice." Journal of Neurophysiology 64, no. 1 (July 1, 1990): 46–56. http://dx.doi.org/10.1152/jn.1990.64.1.46.
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1. Current and voltage-clamp recording of CA3/CA4 pyramidal neurons, hilar neurons, and granule cells or pairs of these neurons were used to study the generation of Cl-dependent and K-dependent inhibitory postsynaptic potentials (IPSPs) in the guinea pig hippocampal slice preparation. 2. A sequence of an early Cl-dependent and a late K-dependent IPSP was evoked in CA3 neurons by electrical stimulation from the stratum moleculare of the dentate gyrus, the hilus, and the stratum oriens/alveus. Blockade of glutamatergic excitation by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and D(-)-2-amino-5-phosphonovaleric acid (APV, 30 microM) abolished IPSPs evoked from the stratum moleculare of the dentate gyrus, but IPSPs could still be evoked from the hilus and the stratum oriens/alveus. 3. Repetitive giant IPSPs, which consisted of Cl-dependent and K-dependent components, were evoked by bath application of 4-aminopyridine (4-AP, 10-50 microM) in CA3 neurons and in granule cells. Giant IPSPs were blocked by bath-applied tetrodotoxin (TTX). In addition, 4-AP hyperpolarized CA3 neurons in a Cl-dependent and picrotoxin-sensitive way. 4. Focal application of TTX to the dentate gyrus or the hilus considerably reduced the amplitude of giant IPSPs evoked by 4-AP in CA3 neurons. In hilar neurons, 4-AP evoked repetitive bursts, eventually, but not necessarily intermingled with giant IPSPs. Bursts were observed in hilar neurons in presence as well as absence of CNQX and APV. 5. In paired recordings, bursts in hilar neurons induced by 4-AP occurred simultaneously to giant IPSPs in granule cells and CA3 neurons, and giant IPSPs in granule cells occurred simultaneously to giant IPSPs in CA3 neurons. Blockade of glutamatergic excitation by CNQX and APV did not abolish this synchrony. 6. 4-AP-evoked Cl- and K-dependent IPSPs were, unlike electrically evoked IPSPs, not strictly coupled: some 20% of large IPSPs and up to 90% of small IPSPs were either Cl or K dependent. In granule cells K-dependent components either preceded or followed Cl-dependent components. 7. K-dependent IPSPs only could be evoked in CA3 neurons by focal application of 4-AP (1 mM) to the hilus, the stratum lacunosum moleculare or the stratum pyramidale. Wash out of Ca for 15–20 min blocked the Cl-dependent but not the K-dependent component of giant IPSPs evoked by bath-applied 4-AP.(ABSTRACT TRUNCATED AT 400 WORDS)
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Sun, Qian, Yu-Qiu Jiang, and Melissa C. Lu. "Topographic heterogeneity of intrinsic excitability in mouse hippocampal CA3 pyramidal neurons." Journal of Neurophysiology 124, no. 4 (October 1, 2020): 1270–84. http://dx.doi.org/10.1152/jn.00147.2020.
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Area CA3 is a major hippocampal region that is classically thought to act as a homogeneous neural network vital for spatial navigation and episodic memories. Here, we report that CA3 pyramidal neurons exhibit marked heterogeneity of somatodendritic morphology and cellular electrical properties along both proximodistal and dorsoventral axes. These new results uncover a complex, yet orderly, pattern of topographic organization of CA3 neuronal features that may contribute to its in vivo functional diversity.
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Menke, Amélie F., Fatme Seval Ismail, Klaus Dornmair, Manuela Cerina, Sven G. Meuth, and Nico Melzer. "GABAA Receptor Autoantibodies Decrease GABAergic Synaptic Transmission in the Hippocampal CA3 Network." International Journal of Molecular Sciences 23, no. 7 (March 28, 2022): 3707. http://dx.doi.org/10.3390/ijms23073707.
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Autoimmune encephalitis associated with antibodies (Abs) against α1, β3, and γ2 subunits of γ-aminobutyric acid receptor A (GABAAR) represents a severe form of encephalitis with refractory seizures and status epilepticus. Reduction in inhibitory GABAergic synaptic activity is linked to dysfunction of neuronal networks, hyperexcitability, and seizures. The aim in this study was to investigate the direct pathogenic effect of a recombinant GABAAR autoantibody (rAb-IP2), derived from the cerebrospinal fluid (CSF) of a patient with autoimmune GABAAR encephalitis, on hippocampal CA1 and CA3 networks. Acute brain slices from C57BL/6 mice were incubated with rAb-IP2. The spontaneous synaptic GABAergic transmission was measured using electrophysiological recordings in voltage-clamp mode. The GABAAR autoantibody rAb-IP2 reduced inhibitory postsynaptic signaling in the hippocampal CA1 pyramidal neurons with regard to the number of spontaneous inhibitory postsynaptic currents (sIPSCs) but did not affect their amplitude. In the hippocampal CA3 network, decreased number and amplitude of sIPSCs were detected, leading to decreased GABAergic synaptic transmission. Immunohistochemical staining confirmed the rAb-IP2 bound to hippocampal tissue. These findings suggest that GABAAR autoantibodies exert direct functional effects on both hippocampal CA1 and CA3 pyramidal neurons and play a crucial role in seizure generation in GABAAR autoimmune encephalitis.
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Ohta, Shinsuke, Shigeru Furuta, Ichiro Matsubara, Keiji Kohno, Yoshiaki Kumon, and Saburo Sakaki. "Calcium Movement in Ischemia-Tolerant Hippocampal CA1 Neurons after Transient Forebrain Ischemia in Gerbils." Journal of Cerebral Blood Flow & Metabolism 16, no. 5 (September 1996): 915–22. http://dx.doi.org/10.1097/00004647-199609000-00015.
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Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracelluar Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca2+-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca2+-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca2+-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequestration and plasma membrane Ca2+-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.
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Wu, Chiping, Marjan Nassiri Asl, Jesse Gillis, Frances K. Skinner, and Liang Zhang. "An In Vitro Model of Hippocampal Sharp Waves: Regional Initiation and Intracellular Correlates." Journal of Neurophysiology 94, no. 1 (July 2005): 741–53. http://dx.doi.org/10.1152/jn.00086.2005.
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During slow wave sleep and consummatory behaviors, electroencephalographic recordings from the rodent hippocampus reveal large amplitude potentials called sharp waves. The sharp waves originate from the CA3 circuitry and their generation is correlated with coherent discharges of CA3 pyramidal neurons and dependent on activities mediated by AMPA glutamate receptors. To model sharp waves in a relatively large hippocampal circuitry in vitro, we developed thick (1 mm) mouse hippocampal slices by separating the dentate gyrus from the CA2/CA1 areas while keeping the functional dentate gyrus-CA3-CA1 connections. We found that large amplitude (0.3–3 mV) sharp wave-like field potentials occurred spontaneously in the thick slices without extra ionic or pharmacological manipulation and they resemble closely electroencephalographic sharp waves with respect to waveform, regional initiation, pharmacological manipulations, and intracellular correlates. Through measuring tissue O2, K+, and synaptic and single cell activities, we verified that the sharp wave-like potentials are not a consequence of anoxia, nonspecific elevation of extracellular K+ and dissection-related tissue damage. Our data suggest that a subtle but crucial increase in the CA3 glutamatergic activity effectively recruits a population of neurons thus responsible for the generation of the sharp wave-like spontaneous field potentials in isolated hippocampal circuitry.
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Harata, Nobutoshi, Jiro Katayama, Yasushi Takeshita, Yoshinaka Murai, and Norio Akaike. "Two components of CA3 pyramidal neurons of the rat." Brain Research 711, no. 1-2 (March 1996): 223–33. http://dx.doi.org/10.1016/0006-8993(95)01406-3.
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McLean, H. A., O. Caillard, R. Khazipov, Y. Ben-Ari, and J. L. Gaiarsa. "Spontaneous release of GABA activates GABAB receptors and controls network activity in the neonatal rat hippocampus." Journal of Neurophysiology 76, no. 2 (August 1, 1996): 1036–46. http://dx.doi.org/10.1152/jn.1996.76.2.1036.
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1. We investigated the effects of the selective gamma-aminobutyric acid-B (GABAB) receptor antagonist, P-3 aminopropyl-P-diethoxymethyl phosphoric acid (CGP 35348), on spontaneous and evoked postsynaptic potentials (PSPs) and currents (PSCs) in CA3 pyramidal cells and interneurons of hippocampal slices obtained between postnatal day 3 and 7 with the use of intracellular and whole cell recording techniques. The intracellular pipette solution contained either 2 M CsCl or 50 mM 2(triethylamino)-N-(2,6-dimethylphenyl) acetamine (QX314) dissolved in 2 M KMeSO4. Cesium and QX314 block postsynaptic responses mediated by GABAB receptors. 2. Under control conditions, bath application of CGP 35348 (0.5-1 mM) progressively increased the duration of spontaneous and evoked polysynaptic giant GABAergic PSPs leading to the appearance of ictal-like discharges. The effects of CGP 35348 were dose dependent and voltage independent. 3. In CA3 pyramidal neurons, CGP 35348 (0.5 mM) had no effect on monosynaptic GABAergic inhibitory PSPs (IPSPs) that were isolated in the presence of ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and D(-)2-amino-5-phosphovaleric acid (D-APV, 50 microM). Similarly, CGP 35348 (0.5 mM) had no effect on monosynaptic glutamatergic excitatory PSPs (EPSPs) that were isolated in the presence of bicuculline (10 microM) and high divalent cation artificial cerebrospinal fluid (ACSF; 6 mM Mg2+/4 mM Ca2+). 4. In CA3 pyramidal neurons exposed to CNQX (20 microM) and D-APV (50 microM), application of the potassium channel blocker 4-aminopyridine (4-AP, 50 microM) generated synchronous giant GABAergic PSPS that were blocked in the presence of high divalent cation ACSF (6 mM Mg2+/4 mM Ca2+) or bicuculline (10 microM). The duration of these synchronous GABAergic PSPs was prolonged in the presence of CGP 35348 (0.5 mM) but did not lead to the appearance of ictal-like discharges. 5. In the presence of bicuculline, interictal giant glutamatergic potentials were observed in simultaneously recorded CA3 pyramidal cells and interneurons. CGP 35348 (0.5 mM) progressively increased the duration of these bicuculline-induced glutamatergic bursts leading to the simultaneous appearance of ictal discharges in both pyramidal cells and interneurons. 6. These results suggest that in the neonatal CA3 hippocampal region, when synchronous giant polysynaptic GABAergic PSPs are present (i.e., under basal, control conditions), spontaneously released GABA reaches a critical level and activates GABAB receptors on both pyramidal cells and interneurons thus regulating the level of glutamatergic and GABAergic activity in the CA3 neuronal network.
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Traynelis, S. F., and R. Dingledine. "Potassium-induced spontaneous electrographic seizures in the rat hippocampal slice." Journal of Neurophysiology 59, no. 1 (January 1, 1988): 259–76. http://dx.doi.org/10.1152/jn.1988.59.1.259.
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1. The CA1 region of rat hippocampal slices bathed in 8.5 mM interstitial K+ ([K+]o) exhibited spontaneous 20- to 90-s electrographic seizures at regular intervals of 1–8 min. In these same slices CA3 neurons generated spontaneous interictal bursts that propagated throughout the pyramidal cell subfields. CA1 electrographic seizures contained components reminiscent of discharges recorded in vivo during tonic-clonic motor seizures. The tonic phase lasted 1–10 s, consisted of a sustained depolarization and firing of CA1 pyramidal cells, and was associated with a negative extracellular potential in the cell layer. The clonic phase lasted tens of seconds and was composed of paroxysmal bursts with afterdischarges in pyramidal cells. 2. Electrographic seizures in CA1 were focal in nature in that they did not invade the CA3 region. Moreover, in approximately 85% of all slices the frequency and amplitude of interictal bursts in CA3 did not change during a CA1 seizure. 3. Both the tonic phase and each clonic discharge of an electrographic seizure were triggered synaptically by a CA3 interictal burst. Microlesions of the Schaffer collateral input abolished CA1 seizures in high [K+]o, and electrical stimulation of these afferents, in a pattern designed to mimic interictal input, restored seizures. Likewise, similarly patterned electrical stimulation of these fibers in slices bathed in high [K+]o with the CA3 region removed reliably evoked electrographic seizures with period and duration similar to spontaneous seizures in whole slices. 4. Electrographic seizures but not CA3 interictal bursts could be reversibly abolished by lowering the temperature from 35–37 to 28–30 degrees C or by the competitive N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (5–10 microM). The inactive isomer, L-2-amino-5-phosphonovaleric acid (25 microM) did not eliminate seizures. 5. Neither the frequency nor intensity of interictal bursts recorded in the CA3 region changed in the minute preceding seizure initiation. Thus, although the presence of interictal input from the CA3 region is required for CA1 seizure generation, it appears that electrographic seizures do not result from a change in the quality or quantity of interictal input to the CA1 region. 6. During the 30- to 60-s period leading to a seizure the excitability of CA1 pyramidal cells appeared to increase gradually. Over the interseizure interval both CA1 pyramidal cells and glia gradually depolarized, the intensity of interictal bursts recorded in the CA1 region increased, and the extracellular DC potential recorded in the CA1 cell layer drifted negative.(ABSTRACT TRUNCATED AT 400 WORDS)