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Artículos de revistas sobre el tema "Ischemia, paired pulse facilitation, hippocampus"

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Publicado: 10 de marzo de 2023

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1

Tanaka, E., S. Yasumoto, G. Hattori, S. Niiyama, S. Matsuyama, and H. Higashi. "Mechanisms Underlying the Depression of Evoked Fast EPSCs Following In Vitro Ischemia in Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 86, no. 3 (2001): 1095–103. http://dx.doi.org/10.1152/jn.2001.86.3.1095.

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The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 ± 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 μM) did not change in amplitude during in vitro ischem
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2

Nathan, T., and J. D. Lambert. "Depression of the fast IPSP underlies paired-pulse facilitation in area CA1 of the rat hippocampus." Journal of Neurophysiology 66, no. 5 (1991): 1704–15. http://dx.doi.org/10.1152/jn.1991.66.5.1704.

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1. Intracellular recordings from CA1 pyramidal neurons in the rat hippocampal slice have been used to study synaptic transmission after maximal orthodromic stimulation of the Schaffer collateral-commissural fibers. Paired-pulse stimulation was used to investigate how the first (conditioning) stimulation influenced the response to the second (test) stimulation. 2. When the test stimulation was delivered up to approximately 4 s after the conditioning stimulation, the late phase of the excitatory postsynaptic synaptic potential (EPSP) was increased (“late-phase facilitation”) whereas the fast (f-
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3

Buonomano, Dean V., and Michael M. Merzenich. "Net Interaction Between Different Forms of Short-Term Synaptic Plasticity and Slow-IPSPs in the Hippocampus and Auditory Cortex." Journal of Neurophysiology 80, no. 4 (1998): 1765–74. http://dx.doi.org/10.1152/jn.1998.80.4.1765.

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Buonomano, Dean V. and Michael M. Merzenich. Net interaction between different forms of short-term synaptic plasticity and slow-IPSPs in the hippocampus and auditory cortex. J. Neurophysiol. 80: 1765–1774, 1998. Paired-pulse plasticity is typically used to study the mechanisms underlying synaptic transmission and modulation. An important question relates to whether, under physiological conditions in which various opposing synaptic properties are acting in parallel, the net effect is facilitatory or depressive, that is, whether cells further or closer to threshold. For example, does the net sum
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4

Saviane, Chiara, Leonid P. Savtchenko, Giacomo Raffaelli, Leon L. Voronin, and Enrico Cherubini. "Frequency‐dependent shift from paired‐pulse facilitation to paired‐pulse depression at unitary CA3‐CA3 synapses in the rat hippocampus." Journal of Physiology 544, no. 2 (2002): 469–76. http://dx.doi.org/10.1113/jphysiol.2002.026609.

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5

Sui, Li, and M. E. Gilbert. "Pre- and Postnatal Propylthiouracil-Induced Hypothyroidism Impairs Synaptic Transmission and Plasticity in Area CA1 of the Neonatal Rat Hippocampus." Endocrinology 144, no. 9 (2003): 4195–203. http://dx.doi.org/10.1210/en.2003-0395.

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Abstract Thyroid hormones are essential for neonatal brain development. It is well established that insufficiency of thyroid hormone during critical periods of development can impair cognitive functions. The mechanisms that underlie learning deficits in hypothyroid animals, however, are not well understood. As impairments in synaptic function are likely to contribute to cognitive deficits, the current study tested whether thyroid hormone insufficiency during development would alter quantitative characteristics of synaptic function in the hippocampus. Developing rats were exposed in utero and p
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6

Tanner, Kylie M., Chinyere Obasi, Ian A. Herrick, and L. Stan Leung. "Effects of Propofol on Hippocampal Synaptic Transmission in Behaving Rats." Anesthesiology 93, no. 2 (2000): 463–72. http://dx.doi.org/10.1097/00000542-200008000-00026.

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Background The action of propofol has been studied in vitro and in vivo, but the effects of intravenously administered propofol on synaptic transmission in freely behaving rats have not been studied before. Methods Rats were implanted with recording electrodes in the dentate gyrus and with stimulation electrodes in the medial perforant path (MPP). Paired pulses at different interpulse intervals (IPIs) were delivered to the MPP, and average evoked potentials were recorded in the dentate gyrus before and after a bolus of propofol (10 or 20 mg/kg administered intravenously) or control vehicle was
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7

Ferchmin, P. A., P. G. DiScenna, E. M. Rivera, V. A. Eterović, and T. J. Teyler. "26. Spermine increases paired-pulse facilitation in area CA1 of hippocampus: Effect of calcium." Journal of Neuroscience Methods 52, no. 1 (1994): A12. http://dx.doi.org/10.1016/0165-0270(94)90086-8.

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8

Andreasen, M., and J. J. Hablitz. "Paired-pulse facilitation in the dentate gyrus: a patch-clamp study in rat hippocampus in vitro." Journal of Neurophysiology 72, no. 1 (1994): 326–36. http://dx.doi.org/10.1152/jn.1994.72.1.326.

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1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time o
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9

Takamatsu, Isao, Ayano Iwase, Makoto Ozaki, Tomiei Kazama, Keiji Wada, and Masayuki Sekiguchi. "Dexmedetomidine Reduces Long-term Potentiation in Mouse Hippocampus." Anesthesiology 108, no. 1 (2008): 94–102. http://dx.doi.org/10.1097/01.anes.0000296076.04510.e1.

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Background Dexmedetomidine (Precedex; Abbott Laboratories, Abbott Park, IL) is a selective alpha2-adrenergic agonist that also has affinity for imidazoline receptors. In clinical studies, dexmedetomidine has sedative effects and impairs memory, but the action of dexmedetomidine on synaptic plasticity in the brain has yet to be established. In the present study, the authors investigated the effects of dexmedetomidine on two forms of synaptic plasticity-long-term potentiation (LTP) and paired-pulse facilitation-in the CA1 region of mouse hippocampal slices. Methods The authors recorded Schaffer
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10

Ferchmin, P. A., Vesna A. Eterović, Edna M. Rivera, and Timothy J. Teyler. "Spermine increases paired-pulse facilitation in area CA1 of hippocampus in a calcium-dependent manner." Brain Research 689, no. 2 (1995): 189–96. http://dx.doi.org/10.1016/0006-8993(95)00568-b.

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11

Debanne, D., N. C. Guérineau, B. H. Gähwiler, and S. M. Thompson. "Paired pulse facilitation and depression at unitary excitatory synapses in the rat hippocampus in vitro." Journal of Physiology-Paris 88, no. 6 (1994): 378. http://dx.doi.org/10.1016/0928-4257(94)90044-2.

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12

Cho, In Ha, Lauren C. Panzera, Morven Chin та ін. "The potassium channel subunit Kvβ1 serves as a major control point for synaptic facilitation". Proceedings of the National Academy of Sciences 117, № 47 (2020): 29937–47. http://dx.doi.org/10.1073/pnas.2000790117.

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Analysis of the presynaptic action potential’s (APsyn) role in synaptic facilitation in hippocampal pyramidal neurons has been difficult due to size limitations of axons. We overcame these size barriers by combining high-resolution optical recordings of membrane potential, exocytosis, and Ca2+in cultured hippocampal neurons. These recordings revealed a critical and selective role for Kv1 channel inactivation in synaptic facilitation of excitatory hippocampal neurons. Presynaptic Kv1 channel inactivation was mediated by the Kvβ1 subunit and had a surprisingly rapid onset that was readily appare
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13

Pairojana, Tanita, Sarayut Phasuk, Pavithra Suresh, and Ingrid Y. Liu. "Behavioral and Synaptic Phenotypes of Female Prdx6−/− Mice." Antioxidants 11, no. 6 (2022): 1201. http://dx.doi.org/10.3390/antiox11061201.

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Peroxiredoxin 6 (PRDX6) is expressed throughout the brain, including the hippocampus, where it plays a potential role in synaptic regulation and forming emotional and spatial memories. PRDX6 is predominantly detected in the female mouse’s hippocampus; thus, we investigate the effect of the Prdx6 gene on behavioral phenotypes and synaptic functions using female Prdx6 knockout (Prdx6−/−) mice. Our results demonstrate that female Prdx6−/− mice exhibited anxiety-like behavior, enhanced contextual fear memory, and impaired spatial memory. We also found increased, paired–pulse facilitation ratios, a
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14

Debanne, D., N. C. Guérineau, B. H. Gähwiler, and S. M. Thompson. "Paired-pulse facilitation and depression at unitary synapses in rat hippocampus: quantal fluctuation affects subsequent release." Journal of Physiology 491, no. 1 (1996): 163–76. http://dx.doi.org/10.1113/jphysiol.1996.sp021204.

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15

Vreugdenhil, Martin, John G. R. Jefferys, Marco R. Celio, and Beat Schwaller. "Parvalbumin-Deficiency Facilitates Repetitive IPSCs and Gamma Oscillations in the Hippocampus." Journal of Neurophysiology 89, no. 3 (2003): 1414–22. http://dx.doi.org/10.1152/jn.00576.2002.

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In the hippocampus, the calcium-binding protein parvalbumin (PV) is expressed in interneurons that innervate perisomatic regions. PV in GABAergic synaptic terminals was proposed to limit repetitive GABA release by buffering of “residual calcium.” We assessed the role of presynaptic PV in Ca2+-dependent GABA release in the hippocampus of PV-deficient (PV−/−) mice and wild-type (PV+/+) littermates. Pharmacologically isolated inhibitory postsynaptic currents (IPSCs) were evoked by low-intensity stimulation of the stratum pyramidale and recorded from voltage-clamped CA1 pyramidal neurons. The ampl
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16

Goodell, Dayton J., Tim A. Benke та K. Ulrich Bayer. "Developmental restoration of LTP deficits in heterozygous CaMKIIα KO mice". Journal of Neurophysiology 116, № 5 (2016): 2140–51. http://dx.doi.org/10.1152/jn.00518.2016.

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The Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a major mediator of long-term potentiation (LTP) and depression (LTD), two opposing forms of synaptic plasticity underlying learning, memory and cognition. The heterozygous CaMKIIα isoform KO (CaMKIIα+/−) mice have a schizophrenia-related phenotype, including impaired working memory. Here, we examined synaptic strength and plasticity in two brain areas implicated in working memory, hippocampus CA1 and medial prefrontal cortex (mPFC). Young CaMKIIα+/− mice (postnatal days 12–16; corresponding to a developmental stage well before schizo
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17

Capogna, M., B. H. Gahwiler, and S. M. Thompson. "Calcium-independent actions of alpha-latrotoxin on spontaneous and evoked synaptic transmission in the hippocampus." Journal of Neurophysiology 76, no. 5 (1996): 3149–58. http://dx.doi.org/10.1152/jn.1996.76.5.3149.

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1. The black widow spider venom component, alpha-latrotoxin (alpha-LTx) (< 0.5 nM), increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal CA3 pyramidal cells 14-fold, without changing their amplitude. 2. This action of alpha-LTx was not affected by application of Ca(2+)-free/ethylene glycol-bis(b-aminoethyl ether)-N,N,N',N'-tetraacetic acid-containing saline, 100 microM Cd2+, or 50 microM Gd3+. The increase in mEPSC frequency was thus not due to an influx of Ca2+ into the axon terminal via voltage-dependent Ca2+ channels or alpha-LTx-induced pores. 3.
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18

Nathan, T., M. S. Jensen, and J. D. C. Lambert. "GABAB receptors play a major role in paired-pulse facilitation in area CA1 of the rat hippocampus." Brain Research 531, no. 1-2 (1990): 55–65. http://dx.doi.org/10.1016/0006-8993(90)90757-3.

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19

A. Samara, Maria, George D. Oikonomou, George Trompoukis, Georgia Madarou, Maria Adamopoulou, and Costas Papatheodoropoulos. "Septotemporal variation in modulation of synaptic transmission, paired-pulse ratio and frequency facilitation/depression by adenosine and GABAB receptors in the rat hippocampus." Brain and Neuroscience Advances 6 (January 2022): 239821282211063. http://dx.doi.org/10.1177/23982128221106315.

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Short-term synaptic plasticity represents a fundamental mechanism in neural information processing and is regulated by neuromodulators. Here, using field recordings from the CA1 region of adult rat hippocampal slices, we show that excitatory synaptic transmission is suppressed by strong but not moderate activation of adenosine A1 receptors by 2-Chloro-N6-cyclopentyladenosine (CCPA) more in the dorsal than the ventral hippocampus; in contrast, both mild and strong activation of GABAB receptors by baclofen (1 μM, 10 μM) suppress synaptic transmission more in the ventral than the dorsal hippocamp
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20

Colgin, Laura Lee, Enikö A. Kramár, Christine M. Gall, and Gary Lynch. "Septal Modulation of Excitatory Transmission in Hippocampus." Journal of Neurophysiology 90, no. 4 (2003): 2358–66. http://dx.doi.org/10.1152/jn.00262.2003.

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Application of the acetylcholinesterase inhibitor physostigmine to conventional hippocampal slices caused a significant reduction of field excitatory postsynaptic potentials (EPSPs) elicited by single pulse stimulation to the medial perforant path. Similar but smaller effects were obtained in the lateral perforant path and other excitatory pathways within hippocampus. The reductions were blocked by atropine, were not accompanied by evident changes in the EPSP waveform, and were eliminated by lesions to the cholinergic septo-hippocampal projections. Antidromic responses to mossy fiber stimulati
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21

Wasling, P., E. Hanse, and B. Gustafsson. "Developmental Changes in Release Properties of the CA3-CA1 Glutamate Synapse in Rat Hippocampus." Journal of Neurophysiology 92, no. 5 (2004): 2714–24. http://dx.doi.org/10.1152/jn.00464.2004.

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Developmental changes in release probability ( Pr) and paired–pulse plasticity at CA3-CA1 glutamate synapses in hippocampal slices of neonatal rats were examined using field excitatory postsynaptic potential (EPSP) recordings. Paired-pulse facilitation (PPF) at these synapses was, on average, absent in the first postnatal week but emerged and became successively larger during the second postnatal week. This developmental increase in PPF was associated with a reduction in Pr, as indicated by the slower progressive block of the N-methyl-d-aspartate (NMDA) EPSP by the noncompetitive NMDA receptor
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22

Clark, K. A., A. D. Randall, and G. L. Collingridge. "A comparison of paired-pulse facilitation of AMPA and NMDA receptor-mediated excitatory postsynaptic currents in the hippocampus." Experimental Brain Research 101, no. 2 (1994): 272–78. http://dx.doi.org/10.1007/bf00228747.

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23

Stubblefield, Elizabeth A., and Tim A. Benke. "Distinct AMPA-Type Glutamatergic Synapses in Developing Rat CA1 Hippocampus." Journal of Neurophysiology 104, no. 4 (2010): 1899–912. http://dx.doi.org/10.1152/jn.00099.2010.

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We assessed synaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) properties during synaptogenesis to describe the development of individual glutamatergic synapses on rat hippocampal CA1 principal neurons. Pharmacologically isolated AMPAR-mediated glutamatergic synaptic currents [evoked by stimulation of the Schaffer Collateral pathway, excitatory postsynaptic currents (EPSCs)], had significantly greater inward-rectification at ages P5–7 compared with P8–18. These inward rectifying EPSCs demonstrated paired-pulse dependent unblocking at positive holding potentials, consis
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24

Cazakoff, Brittany N., and John G. Howland. "Acute stress disrupts paired pulse facilitation and long-term potentiation in rat dorsal hippocampus through activation of glucocorticoid receptors." Hippocampus 20, no. 12 (2010): 1327–31. http://dx.doi.org/10.1002/hipo.20738.

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25

Kudryashova, I. V., I. E. Kudryashov, and N. V. Gulyaeva. "Long-term potentiation in the hippocampus in conditions of inhibition of caspase-3: Analysis of facilitation in paired-pulse stimulation." Neuroscience and Behavioral Physiology 36, no. 8 (2006): 817–24. http://dx.doi.org/10.1007/s11055-006-0092-y.

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26

Pofantis, Hermes, Panagiotis Georgopoulos, Theodoros Petrides, and Costas Papatheodoropoulos. "Differences in paired-pulse inhibition and facilitation in the dentate gyrus and CA3 field between dorsal and ventral rat hippocampus." Brain Research 1608 (May 2015): 21–30. http://dx.doi.org/10.1016/j.brainres.2015.03.003.

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27

Voronin, L. L., A. V. Rossokhin, and M. V. Sokolov. "Intracellular studies of the interaction between paired-pulse facilitation and the delayed phase of long-term potentiation in the hippocampus." Neuroscience and Behavioral Physiology 29, no. 3 (1999): 347–54. http://dx.doi.org/10.1007/bf02465348.

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28

Zhang, Yuchun, Ping Deng, Yan Li, and Zao C. Xu. "Enhancement of Excitatory Synaptic Transmission in Spiny Neurons After Transient Forebrain Ischemia." Journal of Neurophysiology 95, no. 3 (2006): 1537–44. http://dx.doi.org/10.1152/jn.01166.2005.

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Spiny neurons in the neostriatum are highly vulnerable to ischemia. Enhancement of excitatory synaptic transmissions has been implicated in ischemia-induced excitotoxic neuronal death. Here we report that evoked excitatory postsynaptic currents in spiny neurons were potentiated after transient forebrain ischemia. The ischemia-induced potentiation in synaptic efficacy was associated with an enhancement of presynaptic release as demonstrated by an increase in the frequency of miniature excitatory postsynaptic currents (mEPSCs) and a decrease in the paired-pulse ratio. The amplitude of inward cur
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29

Sun, H. Y., A. F. Bartley, and L. E. Dobrunz. "Calcium-Permeable Presynaptic Kainate Receptors Involved in Excitatory Short-Term Facilitation Onto Somatostatin Interneurons During Natural Stimulus Patterns." Journal of Neurophysiology 101, no. 2 (2009): 1043–55. http://dx.doi.org/10.1152/jn.90286.2008.

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Schaffer collateral synapses in hippocampus show target-cell specific short-term plasticity. Using GFP-expressing Inhibitory Neuron (GIN) transgenic mice that express enhanced green fluorescent protein (EGFP) in a subset of somatostatin-containing interneurons (SOM interneurons), we previously showed that Schaffer collateral synapses onto SOM interneurons in stratum (S.) radiatum have unusually large (up to 6-fold) paired-pulse facilitation. This results from a low initial release probability and the enhancement of facilitation by synaptic activation of presynaptic kainate receptors. Here we f
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30

Son, Hyeon, and David O. Carpenter. "Interactions among paired-pulse facilitation and post-tetanic and long-term potentiation in the mossy fiber-CA3 pathway in rat hippocampus." Synapse 23, no. 4 (1996): 302–11. http://dx.doi.org/10.1002/(sici)1098-2396(199608)23:4<302::aid-syn8>3.0.co;2-b.

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31

Fischer, Marc, Julia Reuter, Florian J. Gerich, et al. "Enhanced Hypoxia Susceptibility in Hippocampal Slices From a Mouse Model of Rett Syndrome." Journal of Neurophysiology 101, no. 2 (2009): 1016–32. http://dx.doi.org/10.1152/jn.91124.2008.

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Rett syndrome is a neurodevelopmental disorder caused by mutations in the X-chromosomal MECP2 gene encoding for the transcriptional regulator methyl CpG binding protein 2 (MeCP2). Rett patients suffer from episodic respiratory irregularities and reduced arterial oxygen levels. To elucidate whether such intermittent hypoxic episodes induce adaptation/preconditioning of the hypoxia-vulnerable hippocampal network, we analyzed its responses to severe hypoxia in adult Rett mice. The occurrence of hypoxia-induced spreading depression (HSD)—an experimental model for ischemic stroke—was hastened in Me
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32

González-H, Guillermo, Itzel Jatziri Contreras-García, Karla Sánchez-Huerta, et al. "Levetiracetam Reduced the Basal Excitability of the Dentate Gyrus without Restoring Impaired Synaptic Plasticity in Rats with Temporal Lobe Epilepsy." Brain Sciences 10, no. 9 (2020): 634. http://dx.doi.org/10.3390/brainsci10090634.

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Temporal lobe epilepsy (TLE), the most common type of focal epilepsy, affects learning and memory; these effects are thought to emerge from changes in synaptic plasticity. Levetiracetam (LEV) is a widely used antiepileptic drug that is also associated with the reversal of cognitive dysfunction. The long-lasting effect of LEV treatment and its participation in synaptic plasticity have not been explored in early chronic epilepsy. Therefore, through the measurement of evoked field potentials, this study aimed to comprehensively identify the alterations in the excitability and the short-term (depr
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33

Faivre, Emilie, Victor A. Gault, Bernard Thorens, and Christian Hölscher. "Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis." Journal of Neurophysiology 105, no. 4 (2011): 1574–80. http://dx.doi.org/10.1152/jn.00866.2010.

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Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released from intestine after a meal, producing a glucose-dependent insulin secretion. The GIP receptor (GIPR) is expressed on pyramidal neurons in the cortex and hippocampus, and GIP is synthesized in a subset of neurons in the brain. However, the role of the GIPR in neuronal signaling is not clear. In this study, we used a mouse strain with GIPR gene deletion (GIPR KO) to elucidate the role of the GIPR in neuronal communication and brain function. Compared with C57BL/6 control mice, GIPR KO mice displayed higher lo
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34

Tidball, Patrick, Hannah V. Burn, Kai Lun Teh, Arturas Volianskis, Graham L. Collingridge, and Stephen M. Fitzjohn. "Differential ability of the dorsal and ventral rat hippocampus to exhibit group I metabotropic glutamate receptor–dependent synaptic and intrinsic plasticity." Brain and Neuroscience Advances 1 (January 1, 2017): 239821281668979. http://dx.doi.org/10.1177/2398212816689792.

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Background: The hippocampus is critically involved in learning and memory processes. Although once considered a relatively homogenous structure, it is now clear that the hippocampus can be divided along its longitudinal axis into functionally distinct domains, responsible for the encoding of different types of memory or behaviour. Although differences in extrinsic connectivity are likely to contribute to this functional differentiation, emerging evidence now suggests that cellular and molecular differences at the level of local hippocampal circuits may also play a role. Methods: In this study,
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35

Nishikawa, Koh-ichi, and M. Bruce MacIver. "Excitatory Synaptic Transmission Mediated by NMDA Receptors Is More Sensitive to Isoflurane than Are Non-NMDA Receptor-mediated Responses." Anesthesiology 92, no. 1 (2000): 228. http://dx.doi.org/10.1097/00000542-200001000-00035.

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Background Effects of volatile anesthetic agents on N-methyl-D-aspartate (NMDA) receptor-mediated excitatory synaptic transmission have not been well characterized. The authors compared effects produced by halothane and isoflurane on electrophysiologic properties of NMDA and non-NMDA receptor-mediated synaptic responses in slices from the rat hippocampus. Methods Field excitatory postsynaptic potentials (fEPSPs) in the CA1 area were recorded with extracellular electrodes after electrical stimulation of Schaffer-collateral-commissural fiber inputs. NMDA or non-NMDA receptor-mediated fEPSPs were
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36

Manabe, T., D. J. Wyllie, D. J. Perkel, and R. A. Nicoll. "Modulation of synaptic transmission and long-term potentiation: effects on paired pulse facilitation and EPSC variance in the CA1 region of the hippocampus." Journal of Neurophysiology 70, no. 4 (1993): 1451–59. http://dx.doi.org/10.1152/jn.1993.70.4.1451.

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1. Whole-cell patch-clamp recordings of excitatory postsynaptic currents (EPSCs) were made from guinea pig hippocampal CA1 pyramidal cells. The sensitivity of paired pulse facilitation (PPF) and EPSC variance to changes in synaptic transmission was investigated and the results were compared with the changes in these parameters evoked by long-term potentiation (LTP). 2. Presynaptic manipulations, such as activation of presynaptic gamma-aminobutyric acid-B receptors by baclofen, blockade of presynaptic adenosine receptors by theophylline, blockade of presynaptic potassium channels by cesium, and
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37

Wu, LG, and P. Saggau. "Presynaptic calcium is increased during normal synaptic transmission and paired-pulse facilitation, but not in long-term potentiation in area CA1 of hippocampus." Journal of Neuroscience 14, no. 2 (1994): 645–54. http://dx.doi.org/10.1523/jneurosci.14-02-00645.1994.

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38

Fernández-Fernández, Diego, Holger Rosenbrock, and Katja S. Kroker. "Inhibition of PDE2A, but not PDE9A, modulates presynaptic short-term plasticity measured by paired-pulse facilitation in the CA1 region of the hippocampus." Synapse 69, no. 10 (2015): 484–96. http://dx.doi.org/10.1002/syn.21840.

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Sullivan, Jane M. "Mechanisms of Cannabinoid-Receptor–Mediated Inhibition of Synaptic Transmission in Cultured Hippocampal Pyramidal Neurons." Journal of Neurophysiology 82, no. 3 (1999): 1286–94. http://dx.doi.org/10.1152/jn.1999.82.3.1286.

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Cannabinoids, such as marijuana, are known to impair learning and memory perhaps through their actions in the hippocampus where cannabinoid receptors are expressed at high density. Although cannabinoid receptor activation decreases glutamatergic synaptic transmission in cultured hippocampal neurons, the mechanisms of this action are not known. Cannabinoid receptor activation also inhibits calcium channels that support neurotransmitter release in these cells, making modulation of these channels a candidate for cannabinoid-receptor–mediated effects on synaptic transmission. Whole cell patch-clam
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40

Albiñana, Elisa, Javier Gutierrez-Luengo, Natalia Hernández-Juarez, et al. "Chondroitin Sulfate Induces Depression of Synaptic Transmission and Modulation of Neuronal Plasticity in Rat Hippocampal Slices." Neural Plasticity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/463854.

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It is currently known that in CNS the extracellular matrix is involved in synaptic stabilization and limitation of synaptic plasticity. However, it has been reported that the treatment with chondroitinase following injury allows the formation of new synapses and increased plasticity and functional recovery. So, we hypothesize that some components of extracellular matrix may modulate synaptic transmission. To test this hypothesis we evaluated the effects of chondroitin sulphate (CS) on excitatory synaptic transmission, cellular excitability, and neuronal plasticity using extracellular recording
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41

Kusakari, Shinya, Fumihito Saitow, Yukio Ago, et al. "Shp2 in Forebrain Neurons Regulates Synaptic Plasticity, Locomotion, and Memory Formation in Mice." Molecular and Cellular Biology 35, no. 9 (2015): 1557–72. http://dx.doi.org/10.1128/mcb.01339-14.

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Shp2 (Src homology 2 domain-containing protein tyrosine phosphatase 2) regulates neural cell differentiation. It is also expressed in postmitotic neurons, however, and mutations of Shp2 are associated with clinical syndromes characterized by mental retardation. Here we show that conditional-knockout (cKO) mice lacking Shp2 specifically in postmitotic forebrain neurons manifest abnormal behavior, including hyperactivity. Novelty-induced expression of immediate-early genes and activation of extracellular-signal-regulated kinase (Erk) were attenuated in the cerebral cortex and hippocampus of Shp2
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42

Shang, Yingchun, Xin Wang, Fangjuan Li, Tao Yin, Jianhai Zhang, and Tao Zhang. "rTMS Ameliorates Prenatal Stress–Induced Cognitive Deficits in Male-Offspring Rats Associated With BDNF/TrkB Signaling Pathway." Neurorehabilitation and Neural Repair 33, no. 4 (2019): 271–83. http://dx.doi.org/10.1177/1545968319834898.

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Background. Growing evidences suggest that brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) plays a key role in the regulation of hippocampal synaptic plasticity in a prenatal stress (PNS) rat model. Repetitive transcranial magnetic stimulation (rTMS) is currently being acknowledged to affect attention and memory in both preclinical and clinical studies, although the mechanism is still unclear. Objective. The current study aimed to explore whether a whole brain rTMS (5 Hz, 14 days) could ameliorate cognitive dysfunction–induced PNS in male offspring, and examine if t
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43

Shors, Tracey J., and Richard F. Thompson. "Acute stress impairs (or induces) synaptic long-term potentiation (LTP) but does not affect paired-pulse facilitation in the stratum radiatum of rat hippocampus." Synapse 11, no. 3 (1992): 262–65. http://dx.doi.org/10.1002/syn.890110311.

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44

Mahmoud, Ghada S., and Lawrence M. Grover. "Growth Hormone Enhances Excitatory Synaptic Transmission in Area CA1 of Rat Hippocampus." Journal of Neurophysiology 95, no. 5 (2006): 2962–74. http://dx.doi.org/10.1152/jn.00947.2005.

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The hippocampus produces growth hormone (GH) and contains GH receptors, suggesting a potential role for GH signaling in the regulation of hippocampal function. In agreement with this possibility, previous investigations have found altered hippocampal function and hippocampal-dependent learning and memory after chronic GH administration or deficiency. In this study we applied GH to in vitro rat hippocampal brain slices, to determine whether GH has short-term effects on hippocampal function in addition to previously documented chronic effects. We found that GH enhanced both AMPA- and NMDA-recept
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45

Roberto, M., T. E. Nelson, C. L. Ur, and D. L. Gruol. "Long-Term Potentiation in the Rat Hippocampus Is Reversibly Depressed by Chronic Intermittent Ethanol Exposure." Journal of Neurophysiology 87, no. 5 (2002): 2385–97. http://dx.doi.org/10.1152/jn.2002.87.5.2385.

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Alcohol exposure induces multiple neuroadaptive changes in the CNS that can have serious long-term consequences on CNS function including cognitive effects and attenuation of learning and memory. The cellular mechanisms underlying the CNS effects of alcohol have yet to be fully elucidated and are likely to depend on the pattern and dose of alcohol exposure. Using electrophysiological recordings from hippocampal slices obtained from control and chronic alcohol-treated rats, we have investigated the effects of a binge pattern of alcohol abuse on synaptic plasticity in the CNS. The alcohol-treate
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46

Maltsev, Alexander V., Natalia V. Bal, and Pavel M. Balaban. "Serine/Threonine Phosphatases in LTP: Two B or Not to Be the Protein Synthesis Blocker-Induced Impairment of Early Phase." International Journal of Molecular Sciences 22, no. 9 (2021): 4857. http://dx.doi.org/10.3390/ijms22094857.

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Dephosphorylation of target proteins at serine/threonine residues is one of the most crucial mechanisms regulating their activity and, consequently, the cellular functions. The role of phosphatases in synaptic plasticity, especially in long-term depression or depotentiation, has been reported. We studied serine/threonine phosphatase activity during the protein synthesis blocker (PSB)-induced impairment of long-term potentiation (LTP). Established protein phosphatase 2B (PP2B, calcineurin) inhibitor cyclosporin A prevented the LTP early phase (E-LTP) decline produced by pretreatment of hippocam
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47

Ma, Long, Gerald Reis, Luis F. Parada, and Erin M. Schuman. "Neuronal NT-3 Is not Required For Synaptic Transmission or Long-Term Potentiation in Area CA1 of the Adult Rat Hippocampus." Learning & Memory 6, no. 3 (1999): 267–75. http://dx.doi.org/10.1101/lm.6.3.267.

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Neurotrophic factors, including BDNF and NT-3, have been implicated in the regulation of synaptic transmission and plasticity. Previous attempts to analyze synaptic transmission and plasticity in mice lacking the NT-3 gene have been hampered by the early death of the NT-3 homozygous knockout animals. We have bypassed this problem by examining synaptic transmission in mice in which the NT-3 gene is deleted in neurons later in development, by crossing animals expressing the CRE recombinase driven by the synapsin I promoter to animals in which the NT-3 gene is floxed. We conducted blind field pot
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48

Kawai, Kensuke, LaRoy P. Penix, Nobutaka Kawahara, Christl A. Ruetzler, and Igor Klatzo. "Development of Susceptibility to Audiogenic Seizures following Cardiac Arrest Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 15, no. 2 (1995): 248–58. http://dx.doi.org/10.1038/jcbfm.1995.31.

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Susceptibility to audiogenic seizures (AGS) was investigated in Sprague–Dawley rats subjected to cardiac arrest cerebral ischemia (CACI), produced by compression of the major cardiac vessels. The onset of AGS was regularly observed 1 day after CACI of &gt;5 min duration. The duration of postischemic susceptibility to AGS was directly related to the density of cerebral ischemia, with 50% of more severely ischemic animals still showing AGS susceptibility 8 weeks after CACI. Lesioning of the inferior colliculi (IC) abolished the onset of AGS; no such effect was observed after lesioning the medial
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49

Kessey, Kofi, and David J. Mogul. "NMDA-Independent LTP by Adenosine A2 Receptor-Mediated Postsynaptic AMPA Potentiation in Hippocampus." Journal of Neurophysiology 78, no. 4 (1997): 1965–72. http://dx.doi.org/10.1152/jn.1997.78.4.1965.

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Kessey, Kofi and David J. Mogul. NMDA-independent LTP by adenosine A2 receptor-mediated postsynaptic AMPA potentiation in hippocampus. J. Neurophysiol. 78: 1965–1972, 1997. The role of adenosine A2 receptors in normal synaptic transmission and tetanus-induced long-term potentiation (LTP) was tested by stimulation of the Schaffer collateral pathway and recording of the field excitatory postsynaptic potential (EPSP) in the CA1 region of rat transverse hippocampal slices. Activation of adenosine A2 receptors with the A2 agonist N 6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)-ethyl]adenosine (DPMA
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50

Terada, Sumio, Tetsuhiro Tsujimoto, Yosuke Takei, Tomoyuki Takahashi, and Nobutaka Hirokawa. "Impairment of Inhibitory Synaptic Transmission in Mice Lacking Synapsin I." Journal of Cell Biology 145, no. 5 (1999): 1039–48. http://dx.doi.org/10.1083/jcb.145.5.1039.

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Deletion of the synapsin I genes, encoding one of the major groups of proteins on synaptic vesicles, in mice causes late onset epileptic seizures and enhanced experimental temporal lobe epilepsy. However, mice lacking synapsin I maintain normal excitatory synaptic transmission and modulation but for an enhancement of paired-pulse facilitation. To elucidate the cellular basis for epilepsy in mutants, we examined whether the inhibitory synapses in the hippocampus from mutant mice are intact by electrophysiological and morphological means. In the cultured hippocampal synapses from mutant mice, re
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