Long-term potentiation in thin hippocampal sections studied by intracellular and extracellular recordings
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Post-tetanic potentiation
Tetanic stimulation
Pyramidal cell
Tetanic stimulation
Post-tetanic potentiation
Pyramidal cell
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Phenytoin (10-100 microM) was studied on excitatory synaptic transmission and post-tetanic potentiation (PTP) in the in vitro rat hippocampus. Synaptic potentials were studied using extracellular, intracellular and single-electrode voltage clamp techniques. Field excitatory postsynaptic potentials were recorded from the apical dendrites of CA1 pyramidal cells after Schaffer collateral stimulation. Intracellularly recorded excitatory postsynaptic potentials and excitatory postsynaptic currents were recorded in CA3 pyramidal cells after mossy fiber stimulation and in the presence of 10 microM picrotoxinin. In the CA1 region, phenytoin elicited a reversible depression of field excitatory postsynaptic potentials as well as reduced the time constant of decay of PTP from 79 sec to 47 sec with no change in the magnitude of potentiation. Higher concentrations of phenytoin (100 microM) had a general depressant effect on both the amplitude and time course of PTP. In CA3 cells, phenytoin (10 microM) reduced the mossy fiber synaptic conductance but did not change its reversal potential. Phenytoin (10 microM) also reduced the time constant of decay of PTP of the mossy fiber to CA3 synapse, while having no effect on the magnitude of potentiation. These results show that therapeutically relevant concentrations of phenytoin depress both low-frequency synaptic transmission and the time course of short-term potentiation. Both actions may be involved in the anticonvulsant properties of phenytoin.
Post-tetanic potentiation
Tetanic stimulation
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Post-tetanic potentiation
Postsynaptic Current
Long-term depression
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The sections in this article are: 1 Types of Synapses 2 Postsynaptic Responses at Excitatory Synapses 2.1 Excitatory Postsynaptic Potential and End-plate Potential 2.2 Equivalent Electrical Circuit 2.3 Synaptic Current and End-plate Current 2.4 Conductance of the Synaptic Membrane During the Transmitter Action 2.5 Generation of the Action Potential 2.6 Equilibrium Potential or Reversal Potential 2.6.1 Measurement of the Reversal Potential 2.6.2 Reversal Potential in Excitatory Synapses 2.7 Ionic Mechanism of the Excitatory Synapses 2.7.1 Electrical Measurements 2.7.2 Tracer Experiments 2.8 Specificity of Ion Pathways 2.9 Elementary Conductance Changes Induced by Acetylcholine Molecules 2.10 Time Course of the Transmitter Action 2.10.1 Release of the Transmitter 2.10.2 Process of the Conductance Change 2.10.3 Removal of the Transmitter 2.10.4 Effect of the Membrane Potential 2.11 Action of Transmitter Substances 2.11.1 Site of Action 2.11.2 Extrasynaptic Receptor 2.11.3 Denervation 2.11.4 Desensitization 2.11.5 Actions of Blocking Agents 3 Postsynaptic Responses at Inhibitory Synapses 3.1 Inhibitory Postsynaptic Potential 3.2 Mode of Action of the Inhibitory Postsynaptic Potential 3.3 Ionic Mechanism of the Postsynaptic Inhibition 3.4 Ion Specificity in the Inhibitory Postsynaptic Membrane 4 Presynaptic Inhibition 5 Amount of Transmitter Released and the Postsynaptic Responses 6 Electrical Transmission Versus Chemical Transmision 6.1 Synaptic Delay 6.2 Direction of the Transmission 6.3 Relative Size of the Presynaptic and Postsynaptic Fibers 6.4 Inhibition
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AN entry of Ca2+ into postsynaptic sites may play a role in the induction of long-term potentiation (LTP) of synaptic transmission in the visual cortex. To test this hypothesis, a Ca2+-chelator was injected into layer II/III neurons of sliced visual cortex obtained from young rats, and excitatory postsynaptic potentials (EPSPs) of these cells to test stimulation of the white matter were observed before and after tetanic stimulation of the same site. To confirm the effectiveness of the tetanus, field potentials reflecting the activities of many cells were recorded with another extracellular electrode. The chelator injection led to long-term depression (LTD) of EPSPs following tetanic stimuli which simultaneously induced LTP of field potentials derived from unchelated cells in most of the slices tested. This suggests that a low concentration of postsynaptic, free Ca2+, when associated with tetanic inputs, may lead to LTD while a rise of Ca2+ may lead to LTP.
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In previous experiments on excitatory synaptic transmission in CA1, temporary (10–20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs; under current clamp) and inhibitory postsynaptic currents (IPSCs; under voltage clamp); 2-DG was applied both in the presence and the absence of antagonists of N-methyl-d-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at ≈30 ms) and later (at ≈140 ms) components of IPSPs or IPSCs: by 35.1 ± 10.25% (mean ± SE; for n = 24, P = 0.0023) and 36.5 ± 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG–induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG–induced LTP of excitatory postsynaptic potentials previously observed in CA1.
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The mathematical model of calcium-dependent posttetanic processes in a dendritic spine of a CA3 hippocampal pyramidal neuron which received excitatory and inhibitory afferents was used for studying the LTP and LTD of inhibitory transmission. It has been demonstrated that the inhibitory synaptic efficacy is defined by GABAa and GABAb dephosphorylation which, in turn, is determined by the Ca(2+)-dependent ratio between the active protein kinases and protein phosphatases. Posttetanic decrease/increase in intracellular Ca2+ concentration (Ca2+p) in respect of pretetanic Ca2+ level results in an increase/decrease in number of dephosphorylated GABA receptors and in the LTP/LTD of the efficacy of inhibitory transmission. The extent of modification depends on the ratio between the concentrations of excitatory and inhibitory transmitters in a synaptic cleft. The extent of inhibitory transmission modification is negligible if GABA concentration is very low or high.
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Microstimulation
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In guinea pig hippocampal slices, stimulation of stratum radiatum during depolarization (with intracellular current injections) of nonspiking cells (presumed to be glia) in the apical dendritic area of CA1 pyramidal neurons resulted in a subsequent long-term potentiation of intracellularly recorded excitatory postsynaptic potentials as well as extracellularly recorded population spikes in the CA1 area. Tetanic stimulation of stratum radiatum resulted in a subsequent prolonged depolarization of the presumed glial cells, and this depolarization was smaller when the tetanus was given during the presence of 2-amino-5-phosphonovalerate or when the slices were exposed to Ca 2+ -free medium containing Mn 2+ and Mg 2+ . These results suggest that glial depolarization is involved as one of the steps in generating long-term potentiation.
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IN guinea pig hippocampal slices, a tetanic stimulation of the stratum radiatimi caused long-term potentiation (LTP) of the excitatory postsynaptic potential (EPSP) but not of the GABAB receptor-mediated slow inhibitory postsynaptic potential (IPSP) in the CAI neurons. In neurons in which Ca2+ was chelated with l, 2-bis(2-amino-phenoxy) ethane N, N, N', N'-tetra-acetic acid (BAPTA) or ethylene-bis(oxyethylenenitrilo)tetra-acetic acid (EGTA), tetanic stimulation of the stratum radiatum caused LTP of the slow IPSP but not of the EPSP. These results indicate that a reciprocal relationship exists between LTP of the EPSP and LTP of the slow IPSP as far as the involvement of the postsynaptic Ca2+ is concerned.
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