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Po-wu Gean - One of the best experts on this subject based on the ideXlab platform.
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activation of metabotropic glutamate receptors in conjunction with Postsynaptic Depolarization triggers a long term depression of the n methyl d aspartate receptor mediated synaptic potential in the rat hippocampus
Journal of Biomedical Science, 1995Co-Authors: Po-wu Gean, Jju Home Lin, Fangchia Chang, Jingjane TsaiAbstract:The mechanism responsible for long-term depression (LTD) of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory Postsynaptic potential (EPSPNMDA) was studied. Intracellular recordings were made from CA1 cells of rat hippocampal slices in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 µM) and picrotoxin (50 µM), which block non-NMDA and GABAA receptors, respectively. Intracellular injections of depolarizing pulses (500 ms, 0.3–0.7 nA) at 1 Hz for 5 min in the absence of synaptic stimulation caused a persistent increase in the amplitude of EPSPNMDA. However, coupling Postsynaptic Depolarization with synaptic activity induced LTD. The EPSPNMDA LTD could be blocked byL-2-amino-3-phosphonopropionic acid (50 µM) or (RS)-α-methyl-4-carboxyphenylglycine (200 µM), specific antagonists for metabotropic glutamate receptors (mGluR). Furthermore, application oftrans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 µM), a specific mGluR agonist, in conjunction with Postsynaptic depolarizing elicited LTD. In contrast, the mGluR agonists quisqualate or t-ACPD when given alone produced a sustained enhancement of EPSPNMDA. Finally, coupled Depolarization did not evoke LTD in slices pretreated with the protein kinase C (PKC) inhibitor calphostin c (60 nM). The present results demonstrate that activation of mGluR is necessary for the induction of LTD of EPSPNMDA and suggest that NMDA receptors are subject to bidirectional regulation by mGluR. Furthermore, the induction of LTD is likely to involve the stimulation of PKC.
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pairing of pre and Postsynaptic activities in hippocampal ca1 neurons induces long term modifications of nmda receptor mediated synaptic potential
Brain Research, 1993Co-Authors: Jju Home Lin, Long Joy Way, Po-wu GeanAbstract:Abstract An in vitro slice preparation of rat hippocampus was used to study the long-term modifications of pharmacologically isolatedN-methyl- d -aspartate (NMDA) receptor-mediated excitatory Postsynaptic potential (EPSPNMDA). Intracellular recordings were made from CA1 pyramidal cells in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μM) and picrotoxin (50 μM) which block non-NMDA and GABAA receptors, respectively. Pairing of low-frequency EPSPNMDA with Postsynaptic Depolarization induced a long-term depression (LTD) of EPSPNMDA. The maximal reduction of EPSPNMDA amplitude amounted to 81.3% of the control 1 min after the pairing. When low-frequency synaptic stimulation was paired with strong Postsynaptic Depolarization, a long-term potentiation (LTP) of EPSPNMDA could be induced. These results suggest that the induction of long-term modifications of EPSPNMDA has at least a Postsynaptic component.
Alex M Thomson - One of the best experts on this subject based on the ideXlab platform.
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ca1 pyramidal to basket and bistratified cell epsps dual intracellular recordings in rat hippocampal slices
The Journal of Physiology, 1998Co-Authors: Afia B Ali, Jim Deuchars, Hannelore Pawelzik, Alex M ThomsonAbstract:1. Dual intracellular recordings in the CA1 region of adult rat hippocampal slices and biocytin filling of synaptically connected cells were used to study the excitatory Postsynaptic potentials (EPSPs) elicited in basket (n = 7) and bistratified interneurones (n = 7) by action potentials activated in simultaneously recorded pyramidal cells. 2. Interneurones could be subdivided according to their electrophysiological properties into classical fast spiking, burst firing, regular spiking and fast spiking cells with a rounded spike after-hyperpolarization. These physiological classes did not, however, correlate with morphological type. EPSPs were not recorded in regular spiking cells. 3. Average EPSP amplitudes were larger in bistratified cells (range, 0.5-9 mV) than in basket cells (range, 0. 15-3.6 mV) and the probability of obtaining a pyramidal cell-interneurone EPSP was also higher for the bistratified cells (1:7) than for the basket cells (1:22). EPSP 10-90 % rise times in bistratified cells (0.7-2 ms) and their widths at half-amplitude (3. 9-11.2 ms) were slightly longer than in basket cells (rise times, 0.4-1.6 ms; half-widths, 2.2-9.7 ms). 4. The majority of these EPSPs (6 of 8 tested) increased in amplitude and duration with Postsynaptic Depolarization, although in two (of 4) basket cells the voltage relation was conventional. 5. All EPSPs tested in both basket (n = 7) and bistratified cells (n = 5) decreased in amplitude with repetitive presynaptic firing. The average amplitudes of second EPSPs elicited within 15 ms of the first were between 34 and 94 % of the average amplitude of the first EPSP. Third and fourth EPSPs in brief trains were further depressed. This depression was associated with an increase in the incidence of apparent failures of transmission indicating a presynaptic locus.
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ca1 pyramid pyramid connections in rat hippocampus in vitro dual intracellular recordings with biocytin filling
Neuroscience, 1996Co-Authors: Jim Deuchars, Alex M ThomsonAbstract:In adult rat hippocampus, simultaneous intracellular recordings from 989 pairs of CA1 pyramidal cells revealed nine monosynaptic, excitatory connections. Six of these pairs were sufficiently stable for electrophysiological analysis. Mean excitatory Postsynaptic potential amplitude recorded at a Postsynaptic membrane potential between -67 and -70 mV was 0.7 +/- 0.5 mV (0.17-1.5 mV), mean 10-90% rise time was 2.7 +/- 0.9 ms (1.5-3.8 ms) and mean width at half-amplitude was 16.8 +/- 4.1 ms (11.6-25 ms). Cells were labelled with biocytin and identified histologically. For one pair that was fully reconstructed morphologically, excitatory Postsynaptic potential average amplitude was 1.5 mV, 10-90% rise time 2.8 ms and width at half-amplitude 11.6 ms (at -67 mV). In this pair, correlated light and electron microscopy revealed that the presynaptic axon formed two synaptic contacts with third-order basal dendrites of the Postsynaptic pyramid, one with a dendritic spine, the other with a dendritic shaft. In the four pairs tested, Postsynaptic Depolarization increased excitatory Postsynaptic potential amplitude and duration. In two, D-2-amino-5-phosphonovalerate (50 microM) reduced the amplitude and duration of the excitatory Postsynaptic potential. The remainder of the excitatory Postsynaptic potential now increased with Postsynaptic hyperpolarization and was abolished by 20 microM 6-cyano-7-nitroquinoxaline-2,3-dione (n = 1). Paired-pulse depression was evident in the four excitatory Postsynaptic potentials tested. This depression decreased with increasing inter-spike interval. These results provide the first combined electrophysiological and morphological illustration of synaptic contacts between pyramidal neurons in the hippocampus and confirm that connections between CA1 pyramidal neurons are mediated by both N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate/kainate receptors.
Hiroki Toyoda - One of the best experts on this subject based on the ideXlab platform.
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nicotine facilitates synaptic depression in layer v pyramidal neurons of the mouse insular cortex
Neuroscience Letters, 2018Co-Authors: Hiroki ToyodaAbstract:The insular cortex is known to play a pivotal role in addiction to nicotine. Long-term depression (LTD) in the central nervous system is a major form of synaptic plasticity which is involved in learning and memory and in various pathological conditions such as nicotine addiction. Until now, effects of nicotine on LTD were mainly examined in the hippocampus and striatum, and there is no report showing the effects of nicotine on LTD in the insular cortex. In the present study, I show for the first time that nicotine facilitates LTD which is induced by combination of presynaptic stimulation with Postsynaptic Depolarization (paired training) in layer 5 pyramidal neurons of the mouse insular cortex using whole-cell patch-clamp recordings. The facilitatory effect of nicotine on LTD was blocked by GABAA receptor antagonists, bicuculline and picrotoxin. Furthermore, blockade of β2-containing nicotinic acetylcholine receptors (nAChRs) prevented the effects of nicotine on LTD. Taken together, these results suggest that in layer 5 pyramidal neurons of the insular cortex, nicotine facilitates LTD through enhancement of GABAergic synaptic transmission, presumably mediated by activation of β2-containing nAChRs. These findings may provide the crucial synaptic basis for the insular cortical changes in nicotine addiction.
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nicotinic activity depresses synaptic potentiation in layer v pyramidal neurons of mouse insular cortex
Neuroscience, 2017Co-Authors: Hajime Sato, Tsutomu Kawano, Dong Xu Yin, Takafumi Kato, Hiroki ToyodaAbstract:The insular cortex is a critical brain region involved in nicotine addiction. However, its specific cellular and synaptic mechanisms underlying nicotine addiction remains largely unknown. In the present study, we examined how nicotine modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex. We also examined which type of neurons express functional nicotinic acetylcholine receptors (nAChRs) in layer V of the insular cortex. We found that nicotine suppresses synaptic potentiation induced by combination of presynaptic stimulation with Postsynaptic Depolarization (paired training). An application of nicotine significantly enhanced both spontaneous excitatory Postsynaptic currents (EPSCs) and inhibitory Postsynaptic currents (IPSCs): the former effect was mediated by activation of β2-containing nAChRs while the latter one was mediated largely by activation of β2-containing nAChRs and to a minor extent by activation of α7-containing nAChRs. The application of nicotine significantly enhanced evoked IPSCs but had no effect on evoked EPSCs. We also found that in layer V of the mouse insular cortex, majority of non-fast-spiking (non-FS) interneurons have β2-containing nAChRs while about half of pyramidal neurons and FS interneurons have functional nAChRs. Blockade of GABAA receptors or β2-containing nAChRs prevented the effects of nicotine on synaptic potentiation. Taken together, these results suggest that in layer V pyramidal neurons of the insular cortex, activation of β2-containing nAChRs expressed in non-FS interneurons suppresses synaptic potentiation through enhancing GABAergic synaptic transmission. These findings provide important insights into the cellular and synaptic mechanisms of insular cortical changes in nicotine addiction.
Scott M. Thompson - One of the best experts on this subject based on the ideXlab platform.
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long term synaptic plasticity between pairs of individual ca3 pyramidal cells in rat hippocampal slice cultures
The Journal of Physiology, 1998Co-Authors: Dominique Debanne, Beat H. Gähwiler, Scott M. ThompsonAbstract:1. Long-term potentiation (LTP) and depression (LTD) were investigated at synapses formed by pairs of monosynaptically connected CA3 pyramidal cells in rat hippocampal slice cultures. 2. An N-methyl-D-aspartate (NMDA) receptor-mediated component of the unitary EPSP, elicited at the resting membrane potential in response to single action potentials in an individual CA3 cell, could be isolated pharmacologically. 3. Associative LTP was induced when single presynaptic action potentials were repeatedly paired with 240 ms Postsynaptic depolarizing pulses that evoked five to twelve action potentials or with single Postsynaptic action potentials evoked near the peak of the unitary EPSP. LTP induction was prevented by an NMDA receptor antagonist. 4. Associative LTD was induced when single presynaptic action potentials were repeatedly elicited with a certain delay after either 240 ms Postsynaptic depolarizing pulses or single Postsynaptic action potentials. The time window within which presynaptic activity had to occur for LTD induction was dependent on the amount of Postsynaptic Depolarization. LTD was induced if single pre- and Postsynaptic action potentials occurred synchronously. 5. Homosynaptic LTD was induced by 3 Hz tetanization of the presynaptic neuron for 3 min and was blocked by an NMDA receptor antagonist. 6. Depotentiation was produced with stimulation protocols that elicit either homosynaptic or associative LTD. 7. Recurrent excitatory synapses between CA3 cells display associative potentiation and depression. The sign of the change in synaptic strength is a function of the relative timing of pre- and Postsynaptic action potentials.
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Asynchronous pre- and Postsynaptic activity induces associative long-term depression in area CA1 of the rat hippocampus in vitro.
Proceedings of the National Academy of Sciences of the United States of America, 1994Co-Authors: Dominique Debanne, Beat H. Gähwiler, Scott M. ThompsonAbstract:Associative long-term depression (LTD) was induced in hippocampal slice cultures with repeated low-frequency (0.3 Hz) stimulation of the Schaffer collateral pathway, only when such stimuli were preceded by intracellular injection of brief depolarizing current pulses in the Postsynaptic CA1 pyramidal cell. The decrease in excitatory Postsynaptic potential amplitude lasted > 30 min, could be reversed by induction of potentiation, could be induced at previously potentiated inputs, was input-specific, and did not require activation or potentiation of other inputs. The magnitude of the depression depended upon the time interval between Depolarization and stimulation and upon the duration of the Depolarization pulse. LTD was not observed in neurons impaled with electrodes containing a Ca2+ chelator. LTD could not be induced in the presence of an N-methyl-D-aspartate receptor antagonist, suggesting that voltage-dependent Ca2+ influx is necessary but not sufficient for LTD induction. We conclude that associative LTD results when synaptic activity follows Postsynaptic Depolarization within a circumscribed time window.
Jju Home Lin - One of the best experts on this subject based on the ideXlab platform.
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activation of metabotropic glutamate receptors in conjunction with Postsynaptic Depolarization triggers a long term depression of the n methyl d aspartate receptor mediated synaptic potential in the rat hippocampus
Journal of Biomedical Science, 1995Co-Authors: Po-wu Gean, Jju Home Lin, Fangchia Chang, Jingjane TsaiAbstract:The mechanism responsible for long-term depression (LTD) of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory Postsynaptic potential (EPSPNMDA) was studied. Intracellular recordings were made from CA1 cells of rat hippocampal slices in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 µM) and picrotoxin (50 µM), which block non-NMDA and GABAA receptors, respectively. Intracellular injections of depolarizing pulses (500 ms, 0.3–0.7 nA) at 1 Hz for 5 min in the absence of synaptic stimulation caused a persistent increase in the amplitude of EPSPNMDA. However, coupling Postsynaptic Depolarization with synaptic activity induced LTD. The EPSPNMDA LTD could be blocked byL-2-amino-3-phosphonopropionic acid (50 µM) or (RS)-α-methyl-4-carboxyphenylglycine (200 µM), specific antagonists for metabotropic glutamate receptors (mGluR). Furthermore, application oftrans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 µM), a specific mGluR agonist, in conjunction with Postsynaptic depolarizing elicited LTD. In contrast, the mGluR agonists quisqualate or t-ACPD when given alone produced a sustained enhancement of EPSPNMDA. Finally, coupled Depolarization did not evoke LTD in slices pretreated with the protein kinase C (PKC) inhibitor calphostin c (60 nM). The present results demonstrate that activation of mGluR is necessary for the induction of LTD of EPSPNMDA and suggest that NMDA receptors are subject to bidirectional regulation by mGluR. Furthermore, the induction of LTD is likely to involve the stimulation of PKC.
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pairing of pre and Postsynaptic activities in hippocampal ca1 neurons induces long term modifications of nmda receptor mediated synaptic potential
Brain Research, 1993Co-Authors: Jju Home Lin, Long Joy Way, Po-wu GeanAbstract:Abstract An in vitro slice preparation of rat hippocampus was used to study the long-term modifications of pharmacologically isolatedN-methyl- d -aspartate (NMDA) receptor-mediated excitatory Postsynaptic potential (EPSPNMDA). Intracellular recordings were made from CA1 pyramidal cells in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μM) and picrotoxin (50 μM) which block non-NMDA and GABAA receptors, respectively. Pairing of low-frequency EPSPNMDA with Postsynaptic Depolarization induced a long-term depression (LTD) of EPSPNMDA. The maximal reduction of EPSPNMDA amplitude amounted to 81.3% of the control 1 min after the pairing. When low-frequency synaptic stimulation was paired with strong Postsynaptic Depolarization, a long-term potentiation (LTP) of EPSPNMDA could be induced. These results suggest that the induction of long-term modifications of EPSPNMDA has at least a Postsynaptic component.