Academic literature on the topic 'CA3 pyramidal neurons'
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Journal articles on the topic "CA3 pyramidal neurons"
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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)
Dissertations / Theses on the topic "CA3 pyramidal neurons"
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LICHERI, VALENTINA. "Modulation of Hyperpolarization-Activated Cation Currents (Ih) by Ethanol in Rat Hippocampal CA3 Pyramidal Neurons." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266622.
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It is well established that ethanol (EtOH), through the interaction with several
membrane proteins, as well as intracellular pathways, is capable to modulate many
neuronal function. Recent reports show that EtOH increases the firing rate of
hippocampal GABAergic interneurons through the positive modulation of the
hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels. This effect
might be consistent with the increase of GABA release from presynaptic terminals
observed in both CA1 and CA3 inhibitory synapses that leads the enhancement of the
GABAergic system induced by EtOH. The activation of HCN produced an inward
currents that are commonly called Ih. Ih play an important role for generating specific
neuronal activities in different brain regions, including specific sub-regions of the
hippocampal formation, such as CA1 and CA3 pyramidal neurons and hippocampal
GABAergic interneurons. The main physiologic effect mediated by HCN-induced Ih is
directed to the control of the neuronal resting membrane potential and action
potential (AP) discharge as well as dampen synaptic integration. Since robust Ih are
also present in CA3 glutamatergic neurons, I here investigated whether the action of
EtOH in the control of CA3 excitability can be correlated with its possible direct
interaction with these cation channels. For this purpose, patch-clamp experiments
were performed in CA3 pyramidal neurons from hippocampal coronal slices obtained
from male Sprague-Dawley rats. The data obtained demonstrated that EtOH is able to
modulate Ih in biphasic manner depending on the concentrations used. Low EtOH
concentrations enhanced Ih amplitude, while high reversibly reduced them. This
biphasic action induced by EtOH reflects on firing rate and synaptic integration. In
addition, in this reports it has been shown that EtOH modulates the function of HCN
channels through interfering with the cAMP/AC/PKA intracellular pathways, an effect
that is mimicked also by other endogenous compounds such as dopamine through D1
receptors activation. These data suggest that the HCN-mediated Ih currents in CA3
pyramidal neurons are sensitive to EtOH action, which at low or relevant
concentrations is able to increase or reduce their function respectively. Altogether
these data suggest a potential new mechanism of EtOH actions on hippocampal
formation and may help to better understand the depressant central activity showed
by this drug of abuse
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Dennis, Siobhan Dennis. "An investigation of the effects of oxygen glucose deprivation on glutamate receptor localisation within hippocampal CA3 pyramidal neurons." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544384.
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Küffner, Mercedes [Verfasser], and Michael [Akademischer Betreuer] Frotscher. "Ultrastructural analysis of spine apparatus in CA3 pyramidal neurons following single cell electroporation in Synaptopodin Knockout - mice = Elektronenmikroskopische Untersuchung des Spine-Apparats in CA3 Pyramidenzellen mittels Einzelzell-Elektroporation in Synaptopodin-defizienten Mäusen." Freiburg : Universität, 2013. http://d-nb.info/1115495283/34.
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Caiati, Maddalena Delma. "Activity-dependent regulation of GABA release at immature mossy fibers-CA3 synapses: role of the Prion protein." Doctoral thesis, SISSA, 2012. http://hdl.handle.net/20.500.11767/4719.
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In adulthood, mossy fibers (MFs), the axons of granule cells of the dentate gyrus (DG), release glutamate onto CA3 principal cells and interneurons. In contrast, during the first week of postnatal life MFs release -aminobutyric acid (GABA), which, at this early developmental stage exerts a depolarizing and excitatory action on targeted cells. The depolarizing action of GABA opens voltage-dependent calcium channels and NMDA receptors leading to calcium entry and activation of intracellular signaling pathways involved in several developmental processes, thus contributing to the refinement of neuronal connections and to the establishment of adult neuronal circuits. The release of GABA has been shown to be down regulated by several neurotransmitter receptors which would limit the enhanced excitability caused by the excitatory action of GABA. It is worth noting that the immature hippocampus exhibits spontaneous correlated activity, the so called giant depolarizing potentials or GDPs that act as coincident detector signals for enhancing synaptic activity, thus contributing to several developmental processes including synaptogenesis. GDPs render the immature hippocampus more prone to seizures. Here, I explored the molecular mechanisms underlying synaptic transmission and activity-dependent synaptic plasticity processes at immature GABAergic MF-CA3 synapses in wild-type rodents and in mice lacking the prion protein (Prnp0/0 mice).
In the first paper, I studied the functional role of kainate receptors (KARs) in regulating GABA release from MF terminals. Presynaptic KARs regulate synaptic transmission in several brain areas and play a central role in modulating glutamate release at adult MF-CA3 synapses. I found that functional presynaptic GluK1 receptors are present on MF terminals where they down regulate GABA release. Thus, application of DNQX or UBP 302, a selective antagonist for GluK1 receptors, strongly increased the amplitude of MF-GABAA-mediated postsynaptic currents (GPSCs). This effect was associated with a decrease in failure rate and increase in PPR, indicating a presynaptic type of action.
GluK1 receptors were found to be tonically activated by glutamate present in the extracellular space, since decreasing the extracellular concentration of glutamate with a glutamate scavenger system prevented their activation and mimicked the effects of KAR antagonists. The depressant effect of GluK1 on GABA release was dependent on pertussis toxin (PTx)-sensitive G protein-coupled kainate receptors since it was prevented when hippocampal slices were incubated in the presence of a solution containing PTx. This effect was presynaptic since application of UBP 302 to cells patched with an intracellular solution containing GDP S still potentiated synaptic responses. In addition, the depressant effect of GluK1 on GABA release was prevented by U73122, which selectively inhibits phospholipase C, downstream to G protein activation. Interestingly, U73122, enhanced the probability of GABA release, thus unveiling the ionotropic type of action of kainate receptors. In line with this, we found that GluK1 receptors enhanced MF excitability by directly depolarizing MF terminals via calcium-permeable cation channels. We also explored the possible involvement of
GluK1 in spike time-dependent (STD) plasticity and we found that GluK1 dynamically regulate the direction of STD-plasticity, since the pharmacological block of this receptor shifted spike-time dependent potentiation into depression. The mechanisms underlying STD-LTD at immature MF-CA3 synapses have been investigated in
detail in the second paper.
STD-plasticity is a Hebbian form of learning which consists in bi-directional modifications of synaptic strength according to the temporal order of pre and postsynaptic spiking. Interestingly, we found that at immature mossy fibers (MF)-CA3 synapses, STD-LTD occurs regardless of the temporal order of stimulation (pre versus post or viceversa). However, as already mentioned, while STD-LTD induced by positive pairing (pre before post) could be shifted into STD-LTP after blocking presynaptic GluK1 receptors, STD-LTD induced by negative pairing (post before pre) relied on the activation of CB1 receptors. At P3 but not at P21, endocannabinoids released by the
postsynaptic cell during spiking-induced membrane depolarization retrogradely activated CB1 receptors, probably expressed on MF terminals and persistently depressed GABA release in the rat hippocampus. Thus, bath application of selective CB1 receptor antagonists prevented STD-LTD.
Pharmacological tools allow identifying anandamide as the endogenous ligand responsible of activity-dependent depressant effect. To further assess whether STD-LTD is dependent on the activation of CB1 receptors, similar experiments were performed on WT-littermates and CB1-KO mice. While in WT mice the pairing protocol produced a persistent depression of MF-GPSCs as in rats, in CB1-KO mice failed to induce LTD. Consistent with these data, in situ hybridization experiments revealed detectable levels of CB1 mRNA in the granule cell layer of P3 but not of P21mice. These experiments strongly suggest that at immature MF-CA3 synapses STD-LTD is mediated by CB1 receptors, probably transiently expressed, during a critical time window, on MF
terminals.
In the third paper, I studied synaptic transmission and activity dependent synaptic plasticity at immature MF-CA3 synapses in mice devoid of the prion protein (Prnp0/0). The prion protein (PrPC) is a conserved glycoprotein widely expressed in the brain and involved in several neuronal processes including neurotransmission. If converted to a conformationally altered form, PrPSc can cause neurodegenerative diseases, such as Creutzfeldt-Jakob disease in humans. Previous studies aimed at characterizing Prnp0/0 mice have revealed only mild behavioral changes, including an impaired
spatial learning, accompanied by electrophysiological and biochemical alterations. Interestingly, PrPC is developmentally regulated and in the hippocampus its expression parallels the maturation of MF. Here, we tested the hypothesis that at immature (P3-P7) MF-CA3 synapses, PrPC interferes with synaptic plasticity processes. To this aim, the rising phase of Giant Depolarizing Potentials (GDPs), a hallmark of developmental networks, was used to stimulate granule cells in the dentate gyrus in such a way that GDPs were coincident with afferent inputs. In WT animals, the pairing procedure induced a persistent increase in amplitude of MF-GPSCs. In contrast, in Prnp0/0 mice, the same protocol produced a long-term depression (LTD). LTP was postsynaptic in origin and required the activation of cAMP-dependent PKA signaling while LTD was presynaptic and was reliant on G protein-coupled GluK1 receptor and protein lipase C downstream to G protein activation.
In addition, at emerging CA3-CA1 synapses of PrPC-deficient mice, stimulation of Schaffer collateral failed to induce LTP, known to be PKA-dependent. Finally, we also found that LTD in Prnp0/0 mice was mediated by GluK1 receptors, since UBP 302 blocked its induction. These data suggest that in the immature hippocampus PrPC controls the direction of synaptic plasticity.
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Marissal, Thomas. "Une approche développementale de l' hétérogénéité fonctionnelle des neurones pyramidaux de CA3." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4001/document.
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Les neurones pyramidaux de la région CA3 de l'hippocampe présentent une diversité morphologique, physiologique, biochimique, mais aussi fonctionnelle. Une partie des caractéristiques des neurones étant acquise pendant le développement, nous avons formulé l'hypothèse que la diversité morpho-fonctionnelle des neurones pyramidaux serait déterminée aux stades embryonnaires. Pour tester cette hypothèse, nous avons utilisé des souris transgéniques pour lesquelles l'expression d'un marqueur fluorescent (GFP) est conditionnée par la date de neurogenèse des neurones glutamatergiques. Nous avons enregistré l'activité des neurones en imagerie calcique et montré que les neurones pyramidaux nés le plus tôt déchargent pendant la phase d'initiation des activités épileptiformes générées par le blocage pharmacologique de la transmission GABAergique rapide. De plus, nous montrons que ces neurones précoces possèdent des propriétés morpho-physiologiques distinctes. Enfin, nous montrons que la stimulation de neurones pyramidaux nés tôt peut générer des activités épileptiformes à des stades immatures lorsqu'ils sont stimulés en groupe, et à des stades juvéniles lorsqu'ils sont stimulés individuellement. Ainsi nous démontrons qu'il existe un lien entre la date de neurogenèse et les propriétés morpho-fonctionnelles des neurones pyramidaux de CA3There is increasing evidence that CA3 pyramidal cells are biochemically, electrophysiologically, morphologically and functionally diverse. As most of these properties are acquired during development, we hypothesized that the heterogeneity of the morphofunctionnal properties of pyramidal cells could be determined at the early stages of life. To test this hypothesis, we used a transgenic mouse line in which we glutamatergic cells are labelled with GFP according to their birth date. Using calcium imaging, we recorded multineuron activity in hippocampal slices and show that early generated pyramidal neurons fire during the build-up phase of epileptiform activities generated in the absence of fast GABAergic transmission. Moreover, we show that early generated pyramidal neurons display distinct morpho-physiological properties. Finally, we demonstrate that early generated neurons can generate epileptiform activities when stimulated as assemblies at immature stages, and when stimulated individually at juvenile stages. Thus we suggest a link between the date of birth and the morpho-functional properties of CA3 pyramidal neurons
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Bialowas, Andrzej. "Nouveaux aspects de la fonction axonale dans le néocortex et l'hippocampe de rat." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM5023.
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Le neurone est une cellule polarisée qui se divise en deux compartiments spécialisés : le compartiment somato-dendritique et le compartiment axonal. Généralement, le premier reçoit l'information en provenance d'autres neurones et le second génère un message en sortie lorsque la somme des entrées dépasse une valeur seuil au segment initial de l'axone. Ce signal de nature discrète appelé potentiel d'action (PA) est propagé activement jusqu'à la terminaison synaptique où il déclenche la transmission chimique de l'information. Cependant, la fonction axonale ne se résume pas à la simple transmission des séquences de PA à l'image d'un câble de télégraphe. L'axone est également capable de transmettre des variations continues de signaux électriques infraliminaires dit analogues et les combiner avec l'information digitale véhiculée par le PA. J'ai consacré la majorité de mon travail de thèse à l'étude de ce nouvel aspect de la fonction axonale dans le cadre de la transmission synaptique entre les neurones pyramidaux au sein du réseau excitateur CA3 de l'hippocampe de rat. Les résultats obtenus à partir d'enregistrements de paires de neurones pendant ma thèse mettent en évidence deux sortes de signalisation analogue et digitale qui aboutissent à la facilitation de la transmission synaptique. La facilitation analogue-digitale (FAD) a été observée lors d'une dépolarisation prolongée, mais également à la suite d'une hyperpolarisation transitoire au niveau du corps cellulaire. Ce sont deux versants d'une même plasticité à court-terme qui découle de l'état biophysique des canaux ioniques sensibles au voltage étant à l'origine du PAThe neuron is a polarised cell divided into two specialized compartments: the somato-dendritic and the axonal compartment. Generally, the first one receives information arriving from other neurones and the second generates an output message, when the sum of inputs exceeds a threshold value at the axon initial segment. This all-or-none signal, called the action potential (AP) is propagated actively to the synaptic terminal where it triggers chemical transmission of information. However, axonal function is not limited to transmission of AP sequences like a telegraph cable. The axon is also capable of transmitting continuously changing sub-threshold electric signals called analogue signals and to combine them with the digital information carried by the AP. I devoted the majority of my thesis work to the study of these novel aspects of axonal function in the framework of synaptic transmission between pyramidal neurons in the CA3 excitatory network of the rat hippocampus. The results obtained through paired recordings brought to light two kinds of analogue and digital signalling that lead to a facilitation of synaptic transmission. Analogue-digital facilitation (ADF) was observed during prolonged presynaptic depolarization and also after a transient hyperpolarization of the neuronal cell body. These are two sides of the same form of short-term synaptic plasticity depending on the biophysical state of voltage gated ion channels responsible for AP generation. The first variant of ADF induced by depolarization (ADFD) is due to AP broadening and involves Kv1 potassium channels
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MANIEZZI, CLAUDIA. "Oxytocin modulates GABAA receptor-mediated inhibition onto CA1 pyramidal neurons in mouse." Doctoral thesis, Università degli studi di Pavia, 2017. http://hdl.handle.net/11571/1203349.
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Oxytocin (OT) is a neuropeptide that exerts different peripheral and central actions. I aimed at characterizing the neuromodulatory effects of OT in the hippocampus. Electrophysiological experiments were performed on mouse brain slices using the whole-cell patch-clamp technique on pyramidal neurons (PYR) and GABAergic interneurons (INs) located in CA1 stratum pyramidale. The effect of TGOT (Thr4,Gly7-oxytocin), a selective OT receptor (OTR) agonist, was first evaluated on spontaneous inhibitory postsynaptic currents (sIPSC) recorded from PYRs in Otr+/+ mice. TGOT caused a significant decrease in the sIPSC interval and an increase in the sIPSC amplitude; it also caused an increase in the sIPSC time constant of decay: this suggests the involvement of GABAA receptors (GABAAR) located in a perisynaptic position that deactivate slower than synaptic receptors, generating slower sIPSCs. The TGOT-mediated effects were dependent on the activation of OTRs, being abolished by the OTR antagonist SSR126768A; furthermore, TGOT didn’t modulate sIPSCs in Otr-/- mice. Then, we recorded the miniature inhibitory postsynaptic currents (mIPSC), isolated by applying tetrodotoxin, a voltage-gated Na+ channel blocker, to prevent action potential firing in the presynaptic terminal. TGOT was not able to modulate the mIPSC interval, amplitude and kinetics of decay, indicating that the effects elicited by the agonist are dependent on the firing activity of the presynaptic neuron. After having clarified the action of TGOT on ‘phasic’ inhibitory transmission, elicited by synaptic and perisynaptic GABAARs, we enquire if the peptide could influence ‘tonic’ currents, mediated by extrasynaptic GABAARs. First, we demonstrated the presence of tonic currents by measuring the ‘baseline holding current’ required to clamp PYRs at a given potential, in control conditions and during the application of the GABAAR antagonist bicuculline: we observed an inward shift in the ‘baseline holding current’ in the presence of bicuculline, consistent with the abolition of tonic currents. Then, we found that TGOT was able to increase tonic currents, causing an outward shift in the ‘baseline holding current’. Subsequently, we tried to understand the source of that TGOT-mediated increased inhibition, finding that TGOT depolarized mainly the stuttering fast-spiking INs. The same depolarization was observed in the presence of synaptic blockers, suggesting that the effect is due to a direct binding to OTRs. Indeed, the perfusion of the OTR antagonist completely abolished the depolarization. We tried to investigate the ionic mechanism underlying the TGOT-induced depolarization. We tested the putative involvement of a Ca2+ current by using nifedipine, a selective L-type channel blocker. Actually, in the majority of INs examined, nifedipine was able to abolish the depolarization elicited by TGOT. Finally, we investigated the effect of TGOT on the membrane potential of PYRs. Most of them, examined at their spike threshold, became hyperpolarized by TGOT and their firing rate was significantly decreased. The hyperpolarizing response was completely abolished by the blockade of GABAARs, indicating that the effect requires the activation of extrasynaptic GABAARs that mediate a prolonged (or tonic) hyperpolarizing current. The TGOT-mediated hyperpolarization caused a reduction in cell excitability, altering the capability of PYRs to generate action potentials in response to depolarizing current steps. This was evident in the firing rate-to-injected current (F-I) relationship that was shifted to the right during perfusion of TGOT. The gain (i.e., the slope) of the curve was not influenced by TGOT. This behavior indicates an increase in tonically active inhibitory currents that lead to a persistent reduction in the input resistance and therefore in cell excitability.
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Song, Jun. "Neuronal Adaptations in Rat Hippocampal CA1 Neurons during Withdrawal from Prolonged Flurazepam Exposure: Glutamatergic System Remodeling." Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1177519349.
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Thesis (Ph.D.)--University of Toledo, 2007."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Major advisor: Elizabeth Tietz. Includes abstract. Title from title page of PDF document. Bibliography: pages 88-94, 130-136, 178-189, 218-266.
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Nassrallah, Wissam. "Store-Operated Response in CA1 Pyramidal Neurons Exhibits Features of Homeostatic Synaptic Plasticity." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33357.
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Homeostatic synaptic plasticity (HSP) regulates synaptic strength in response to changing neuronal firing patterns. This form of plasticity is defined by neurons’ ability to sense and over time integrate their level of firing activity, and to actively maintain it within a defined range. For instance, a compensatory increase in synaptic strength occurs when neuronal activity is chronically attenuated. However, the underpinning cellular mechanisms of this fundamental neural process remain poorly understood. We previously found that during activity deprivation, HSP leads to an increase in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA) receptor function as well as a shift in subunit composition from Ca2+-impermeable GluA2-containing AMPA receptors to Ca2+-permeable GluA2-lacking AMPA receptors not only at synapses, but also at extrasynaptic sites. Neurons therefore appear to be actively enhancing Ca2+ entry, possibly as a compensatory mechanism in response to a prolonged Ca2+ deficit. To test whether the homeostatic response may, at least in part, be mediated by internal Ca2+ stores, we depleted endoplasmic reticulum (ER) Ca2+ stores by using the Sarco/endoplasmic reticulum Ca2+ ATPases (SERCA) pump blocker cyclopiazonic acid (CPA) for a prolonged period. Interestingly, we have found that prolonged Ca2+-store depletion leads not only to an increase in synaptic strength per se, but also a cell-wide increase in synaptic Ca2+-permeable GluA2-lacking AMPARs. This increase in Ca2+ influx following periods of inactivity is conceptually highly reminiscent of a store-operated response, whereby cells re-establish their calcium levels following Ca2+ store depletion using cell surface Ca2+ channels. Our results suggest that neurons use synaptic receptors as means to regulate store Ca2+ levels, thus significantly expanding our understanding of the repertoire used by neurons to modulate cellular excitability.
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Turner, Ray William. "Action potential discharge in somata and dendrites of CA1 pyramidal neurons of mammalian hippocampus : an electrophysiological analysis." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25989.
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The electrophysiological properties of somatic and dendritic membranes of CA1 pyramidal neurons were investigated using the rat in vitro hippocampal slice preparation. A comprehensive analysis of extracellular field potentials, current-source density (CSD) and intracellular activity has served to identify the site of origin of action potential (AP) discharge in CA1 pyramidal neurons.
1) Action potential discharge of CA1 pyramidal cells was evoked by suprathreshold stimulation of the alveus (antidromic) or afferent synaptic inputs in stratum oriens (SO) or stratum radiatum (SR). Laminar profiles of the "stimulus evoked" extracellular field potentials were recorded at 25µm intervals along the dendro-somatic axis of the pyramidal cell and a 1-dimensional CSD analysis applied.
2) The shortest latency population spike response and current sink was recorded in stratum pyramidale or the proximal stratum oriens, a region corresponding to somata and axon hillocks of CA1 pyramidal neurons. A biphasic positive/negative spike potential (current source/sink) was recorded in dendritic regions, with both components increasing in peak latency through the dendritic field with distance from the border of stratum pyramidale.
3) A comparative intracellular analysis of evoked activity in somatic and dendritic membranes revealed a basic similarity in the pattern of AP discharge at all levels of the dendro-somatic axis. Stimulation of the alveus, SO, or SR evoked a single spike while injection of depolarizing current evoked a repetitive train of spikes grouped for comparative purposes into three basic patterns of AP discharge.
4) Both current and stimulus evoked intracellular spikes displayed a progressive decline in amplitude and increase in halfwidth with distance from the border of stratum pyramidale.
5) The only consistent voltage threshold for intracellular spike discharge was found in the region of the cell body, with no apparent threshold for spike activation in dendritic locations.
6) Stimulus evoked intradendritic spikes were evoked beyond the peak of the population spike recorded in stratum pyramidale, and aligned with the biphasic extradendritic field potential shown through laminar profile analysis to conduct with increasing latency from the cell body layer.
The evoked characteristics of action potential discharge in CA1 pyramidal cells are interpreted to indicate the initial generation of a spike in the region of the soma-axon hillock and a subsequent retrograde spike invasion of dendritic arborizations.Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
Books on the topic "CA3 pyramidal neurons"
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Levine, Michael S., Elizabeth A. Wang, Jane Y. Chen, Carlos Cepeda, and Véronique M. André. Altered Neuronal Circuitry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0010.
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In mouse models of Huntington’s disease (HD), synaptic alterations in the cerebral cortex and striatum are present before overt behavioral symptoms and cell death. Similarly, in HD patients, it is now widely accepted that early deficits can occur in the absence of neural atrophy or overt motor symptoms. In addition, hyperkinetic movements seen in early stages are followed by hypokinesis in the late stages, indicating that different processes may be affected. In mouse models, such behavioral alterations parallel complex biphasic changes in glutamate-mediated excitatory, γ-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and dopamine modulation in medium spiny neurons of the striatum as well as in cortical pyramidal neurons. The progressive electrophysiologic changes in synaptic communication that occur with disease stage in the cortical and basal ganglia circuits of HD mouse models strongly indicate that therapeutic interventions and strategies in human HD must be targeted to different mechanisms in each stage and to specific subclasses of neurons.
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Gaetz, Michael B., and Kelly J. Jantzen. Electroencephalography. Edited by Ruben Echemendia and Grant L. Iverson. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199896585.013.006.
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Axonal injury is currently considered to be the structural substrate behind most concussion-related neurological dysfunction. Because the principal generators of EEG fields are graded excitatory and inhibitory synaptic potentials of pyramidal neurons, the EEG is well suited for characterizing large-scale functional disruptions associated with concussion induced metabolic and neurochemical changes, and for connecting those disruptions to deficits in behavior and cognition. This essay provides an overview of the use of EEG and newly developed analytical procedures for the measurement of functional impairment related to sport concussion. Elevations in delta and theta activity can be expected in a percentage of athletes and change in asymmetry and coherence may also be present. Newer techniques are likely to be of critical importance for understanding the anatomical and physiological basis of cognitive deficits and may provide additional insight into susceptibility to future injury. Computational modeling may advance our understanding of concussion.
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Roze, Emmanuel, and Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.
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GM1 gangliosidosis is due to beta-galactosidase deficiency. The adult-onset form is characterized by progressive generalized dystonia, often associated with akineto-rigid Parkinsonism. Mild skeletal dysplasia and short stature are good diagnostic clues. GM2 gangliosidosis is due to beta-hexosaminidase deficiency. The adult-onset form is characterized by complex neurological disorders, in which features resulting from cerebellar and motor neuron dysfunction are the most frequent. Movement disorders, psychotic symptoms, mild pyramidal signs, axonal polyneuropathy, autonomic dysfunction, and vertical supranuclear palsy can also be observed. Clinical severity and the rate of progression both vary widely from one patient to another. Diagnosis is based on measurements of enzyme activity and molecular analysis. Physiotherapy, speech therapy and management of swallowing are crucial for these patients’ quality of life and prognosis.
Book chapters on the topic "CA3 pyramidal neurons"
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Gaïarsa, J. L., R. Corradetti, Y. Ben-Ari, and E. Cherubini. "GABA Mediated Synaptic Events in Neonatal Rat CA3 Pyramidal Neurons in Vitro: Modulation by NMDA and Non-NMDA Receptors." In Excitatory Amino Acids and Neuronal Plasticity, 151–59. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_18.
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Ruiz, Arnaud. "Kainate Receptors with a Metabotropic Signature Enhance Hippocampal Excitability by Regulating the Slow After-Hyperpolarization in CA3 Pyramidal Neurons." In Advances in Experimental Medicine and Biology, 59–68. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-9557-5_6.
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Poirazi, Panayiota, and Eleftheria-Kyriaki Pissadaki. "The Making of a Detailed CA1 Pyramidal Neuron Model." In Hippocampal Microcircuits, 317–52. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0996-1_11.
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BagheriMofidi, S. M., M. Pouladian, and S. B. Jameie. "Effective Current Dipole Model of CA1 Hippocampus Pyramidal Neurons in Rat." In IFMBE Proceedings, 55–58. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03005-0_15.
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Ma, Dan, Shenquan Liu, and Lei Wang. "Transition of Firing Patterns in a CA1 Pyramidal Neuron Model." In Advances in Cognitive Neurodynamics (III), 817–23. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-4792-0_107.
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Rao, D. G., and A. W. L. Chiu. "Enhance Signal Detection in Auto-Associative CA3 Pyramidal Neuron Model Using Electric Field Noise." In IFMBE Proceedings, 131–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01697-4_46.
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Saudargiene, Ausra, Rokas Jackevicius, and Bruce P. Graham. "Interplay of STDP and Dendritic Plasticity in a Hippocampal CA1 Pyramidal Neuron Model." In Artificial Neural Networks and Machine Learning – ICANN 2017, 381–88. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-68600-4_44.
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Tsubokawa, H., N. Kawai, and W. N. Ross. "Muscarinic Modulation of Na+ Spike Propagation in the Apical Dendrites of Hippocampal CA1 Pyramidal Neurons." In Slow Synaptic Responses and Modulation, 416–19. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66973-9_56.
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Dave, Vijay, Arpit D. Shrimankar, Devanshi Gokani, and Abha Dashora. "Mathematical Modelling of Magnesium Block-Driven NMDA Receptor Response in CA1 Pyramidal Neuron for Alzheimer’s Disease." In Nanoelectronics, Circuits and Communication Systems, 91–100. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7486-3_10.
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Nitatori, T., N. Sato, E. Kominami, and Y. Uchiyama. "Participation of Cathepsins B, H, and L in Perikaryal Condensation of CA1 Pyramidal Neurons Undergoing Apoptosis After Brief Ischemia." In Intracellular Protein Catabolism, 177–85. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0335-0_22.
Full textConference papers on the topic "CA3 pyramidal neurons"
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Xie, Nan, Qingli Qiao, and Dan Wang. "Analysis of membrane dynamics of hippocampal CA1 pyramidal neurons." In 2010 3rd International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2010. http://dx.doi.org/10.1109/bmei.2010.5639613.
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Lorenzo, Jhunlyn, Roman Vuillaume, Steephane Binczak, and Sabir Jacquir. "Identification of Synaptic Integration Mode in CA3 Pyramidal Neuron Model." In 2019 9th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2019. http://dx.doi.org/10.1109/ner.2019.8717136.
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Liu, Hua-Kuang. "Multi-resolution pyramidal image compression via perfect convergent neural associative memory." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/oam.1992.mqq5.
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A multiresolution pyramidal image/data compression technique via the perfect convergent unipolar terminal attractor based associative memory is described. By properly choosing adaptive thresholds for dynamic iteration of the unipolar binary neuron states with an inner-product terminalattractor based neural associative memory,1 it has been demonstrated via computer simulation that perfect convergence and correct retrieval can be achieved.2 The perfect convergence feature of the neural associative memory can be used to reduce a 2D image/data into an image of much smaller dimensions, i.e., if n × n neurons are used as one unit cell, an image of N × N unipolar binary pixels can first be divided into (N/n) × (N/n) cells. For example, each cell can be associatively retrieved into two pre-determined memory vectors that may be considered as belonging to two bit planes. If one of the memory states is assigned a value of 1 and the other is assigned 0, then the combination of the two bit planes yields an image of a dimension being that of the original reduced by n × n. Continuation of the process will yield a pyramidal architecture of reduced image/data of different resolutions. Since in each layer the data features and format are dependent on the memorized vectors chosen, an abundance of choices can be made to tailor for specific needs of image processing applications.
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Castanares, Michael, and Vincent Ricardo Daria. "Holographic multi-site Ca2+ imaging along thin dendrites of cortical pyramidal neurons." In Clinical and Translational Biophotonics. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/translational.2018.jth5a.3.
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Li, Guoshi, Harvey C. Cline, Pierre Blier, and Satish Nair. "Computational Studies of Gain Modification by Serotonin in Pyramidal Neurons of Prefrontal Coxtex." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15080.
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Serotonin (5-HT) is widely implicated in brain functions and diseases, but the cellular mechanisms underlying 5-HT functions in the brain are not well understood (Zhang and Arsenault, 2005). Recent experiments (Zhang and Arsenault, 2005) have shown that 5-HT substantially increased the slope (gain) of the firing rate current (F-I) curve in layer 5 pyramidal neurons of the rat prefrontal cortex and this effect was limited to the range of firing rate (0-10 Hz) that is known to behaviourally relevant. Furthermore, it was found that 5-HT mediated gain increase was due to a reduction of the afterhyperpolarization (AHP) and an induction of the slow afterdepolarization (ADP), regardless of changes in the membrane potential, the input resistance or the properties of action potentials. To investigate this frequency-dependent gain modulation of 5-HT on the prefrontal cortex neurons, conductance-based Hodgkin-Huxley type models of the regular spiking (RS) cells in the prefrontal cortex are developed using a step by step approach. We first show that a model with an A current displays a square-root form F-I curve with higher slope at low frequency. However, for the same range of current injection steps used in experiment, the frequency range goes beyond 20 Hz, suggesting the presence of other hyperpolarizing currents in the model. As suggested by the experiment (Zhang and Arsenault, 2005), AHP currents (fast AHP, medium AHP and slow AHP) are included in the model to simulate 5-HT effect. Simulations show that AHP currents effectively linearize the F-I curve and decrease the slope of F-I curve in general, thus reducing the neuronal excitability. Since the slow AHP current is a target of 5-HT, the strength of this current is reduced gradually and the F-I curves are plotted together for comparison. The results indicate that with decreasing slow AHP strength, the current thresholds for repetitive spiking decreases and the slopes of the F-I curves increase in general. A square-root form F-I curve is not evident until the slow AHP current is blocked completely. This suggests that the medium AHP current also play a role in linearizing the F-I curve besides the slow AHP current. Based on current findings, a full model with both A current and AHP currents is being constructed to match the experimental data more closely so the mechanism of 5-HT on gain modulation of prefrontal cortical neurons can be better understood.
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Reza, F., T. Begum, M. U. Ilmie, M. C. L. Hanif, J. Zhang, and J. M. Abdullah. "Simulation study of the effect of Mitragyna speciosa on hybrid current in rat hippocampus CA3 pyramidal neuron." In 2011 11th International Conference on Hybrid Intelligent Systems (HIS 2011). IEEE, 2011. http://dx.doi.org/10.1109/his.2011.6122122.
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Lin, Zhengrong, Lili Niu, Long Meng, Wei Zhou, Xiaowei Huang, and Hairong Zheng. "Notice of Removal: Ultrasound neuro-modulation chip for activating the pyramidal neurons in hippocampal CA1 slices." In 2017 IEEE International Ultrasonics Symposium (IUS). IEEE, 2017. http://dx.doi.org/10.1109/ultsym.2017.8091609.
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Jang, T. S., J. Nair, S. Nair, and A. Lavin. "Modulation of PFC Pyramidal Cell Excitability by Clonidine: A Computational Modeling Study." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15109.
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The prefrontal cortex (PFC) is critically involved in cognitive processes underlying working memory (WM), attention, and inhibition of responses to non-relevant stimuli (Fuster, 2000; Goldman-Rakic, 1996). In this context, catecholaminergic inputs have proven to be critical for the regulation of these cognitive processes (Levitt et al., 1984; Lewis et al., 1987; Lewis and Morrison, 1989; Porrino and Goldman-Rakic, 1982). Aston-Jones and Bloom (1981a, b) showed that, in addition to dopamine (DA) the norepinephrine (NE) neurons located in the locus coeruleus (LC) and terminating in the PFC are important in mediating selective and sustained attention and vigilance. Moreover, stimulation of the LC increases the discrimination of incoming external stimuli to the PFC by reducing the background noise, therefore enhancing the cortical signal-to-noise ratio (Aston-Jones et al., 1985; Berridge and Waterhouse, 2003; Foote et al., 1980, 1983; Waterhouse et al., 1980; Robbins, 2000). More recently, several studies have shown that adrenergic agonists, especially specific alpha-2 agonists, are very effective in enhancing WM and attention. Indeed, administration of alpha-2 agonists can ameliorate some of the negative effects on cognition produced by NE depletion due to aging in monkeys (Arnsten and Goldman-Rakic, 1985; Arnsten et al., 1988; Arnsten and Leslie, 1991) and improve performance in WM-related tasks in young monkeys with NE depletion (Arnsten and Goldman-Rakic, 1985; Cai et al., 1993). Moreover, the therapeutic effects of the specific alpha-2 agonists, clonidine and guanfacine in treating disorders related to dysfunction of WM in patients have been proved (Fields et al., 1988; Mair and McEntree 1986, 1988; Hunt et al., 1985, 1990, 1995).
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Guelli, Mariana Sandoval Terra Campos, Daniela Bastos de Almeida Zampier, Lorena Araújo Silva Dias, and Marina de Oliveira Nunes Ibrahim. "Creutzfeldt-Jakob Disease - a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.126.
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Background: Creutzfeldt-Jakob disease (CJD) is a progressive, rare, fatal and rapid human neurodegenerative disease that occurs in the etiologies: sporadic (CJD), familial, iatrogenic (CJD) and CJD variant (CJV) in which cell prion protein (PrP) can be transmitted through animals. Objectives: Literature review about Creutzfeldt-Jakob diseaseDesign and setting: Literature review development in the Centro Universitário de Volta Redonda, Rio de Janeiro, Brazil. Methods: The Creutzfeldt-Jakob disease, infectious diseases and neuroinfection indexes were used in the PUBMED and Scielo databases. Results:CJD has different etiologies with different clinical and pathological phenotypes. CJDV shows psychiatric behaviors and symptoms followed by abnormalities, ataxia and dementia. The sporadic form is the most common, with a progressive clinical course with generalized brain deposition of abnormal prion protein aggregates (PrPTSE) that leads to spongiform change, gliosis and neuronal loss. CJD progresses to dementia and two or more symptoms: cerebellar or visual impairments; pyramidal or extrapyramidal signs; myoclonus; and akinetic mutism. Complex periods of acute wave in the electroencephalogram (EEG) are strongly suggestive of prionic diseases. Rapidly evolving field neuroimmune disorders have shown an increasing in autoantibody testing; attempt to diagnose a range of immune-mediated conditions. Evidence indicates that diffusion-weighted magnetic resonance imaging (DWI) is more sensitive for detecting signal abnormalities. Conclusion: The disease progresses to dementia, accompanied by myoclonus, pyramidal signs and characteristic EEG. It is a complex pathology, which has only symptomatic treatment and requires strict control of reservoirs and risk of contamination.
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Svoboda, K., W. Denk, W. H. Knox, and S. Tsuda. "Two-photon excitation scanning microscopy with a compact, mode locked, diode- pumped Cr:LiSAF Laser." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 1996. http://dx.doi.org/10.1364/up.1996.wb.2.
Full textAbstract:
Laser scanning microscopy combined with two-photon excitation of fluorescence holds great promise in imaging biological systems. This two-photon excitation laser scanning microscopy (TPLSM) [1] yields intrinsic submicron three-dimensional resolution with much reduced background fluorescence and thus reduced photodamage. Although the advantages of TPLSM as compared to wide field fluorescence microscopy and confocal microscopy have been demonstrated in a number of applications [2], the large cost and utility requirements of mode locked Ti:sapphire laser systems and other femtosecond light sources have kept TPLSM out of reach for most biology labs. We demonstrate here that a recently developed compact solid state laser that is mode locked with a Saturable Bragg Reflector (SBR) [3] is well-suited for TPLSM. A SBR-modelocked Cr:LiSAF laser was pumped with a 0.5 W, 670 nm diffraction-limited MOPA (SDL), providing 90 fs pulses at 860 nm with CW power of 25-44 mW per beam (Fig. la). A single beam was directed into a laser scanning microscope consisting of a pair of galvomirrors, a relay lens, a dichroic mirror, a Zeiss water-immersion objective (63 x 0.9 NA), and a photomultiplier tube for the detection of fluorescence photons [2]. Rat cortical brain slices (300 μm thick) were prepared using standard techniques. For anatomical imaging, neocortical pyramidal cells that were deeply embedded in the tissue were dialyzed and voltage clamped using whole-cell electrodes containing 500 μM fluorescein dextran (MW = 3 kD). TPLSM imaging at low magnification (Fig. 1B) revealed primary and secondary dendrites and the initial segment of the axon. At high magnification single dendritic spines, the smallest neuronal compartments, became apparent (Fig. 1C, arrow). A series of images acquired at different focal planes (Δz = 1.6 μm) demonstrates the sectioning capabilities of the microscope (Fig. 1D-F). For functional imaging of physiological calcium responses, neurons were dialyzed with electrodes containing the calcium indicator Ca-green-1 (300 μM, Molecular Probes). Ca-green is a fluorophore that undergoes a large fluorescence intensity change in response to Ca2+ binding. Intracellular free calcium concentration changes evoked by single action potentials could easily be detected (Fig. 1G).