[Correlations between spontaneous unit activities and evoked responses of amygdaloid neurons].
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Amygdala↗
Biomedical subjects
Y Ben-Ari
Publications and source records attributed to Y Ben-Ari.
[Study, in cats, during an experimental protocol of sensory habituation, of evolution of histograms of intervals between spikes realized from cellular unities of the amygdala complex].
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Amygdala↗
[Examples of modifications of unit activity obtained in the amygdaloid complex of the cat during sensory-sensorial association].
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Amygdala↗
Effects of kainate on the excitability of rat hippocampal neurones.
Intracellular recordings from CA1 pyramidal neurones of the rat hippocampal slice preparation were used to study changes in neuronal excitability induced by the excitatory amino acid analogues kainate (KA) and N-methyl-D-aspartate (NMDA). Low concentrations of bath-applied KA (50-200 nM) or NMDA (1-3 microM) elicited a relatively small membrane depolarization and increased the number of spikes fired by a constant current pulse. The spike after-hyperpolarization (AHP) was depressed by KA but enhanced by NMDA. After blockade of the voltage-sensitive Na+ conductances with tetrodotoxin, intracellularly applied current pulses elicited Ca2+ spikes. Whereas NMDA always increased the duration (and number) of Ca2+ spikes and of their AHP, KA conversely reduced these spikes and (in almost half of the cells tested) the late phase of their AHP. When Ba2+ was used to replace extracellular Ca2+, prolonged plateau potentials developed and were also blocked by KA. NMDA had no effect on Ba2(+)-dependent responses. These results suggest that low concentrations of KA profoundly modified the electroresponsiveness of CA1 neurones perhaps by depressing a Ca2(+)-dependent K+ conductance mechanism responsible for dampening the excitability of these cells.
Action Potentials↗
Ischemia induces short- and long-term remodeling of synaptic activity in the hippocampus.
One of the most vulnerable areas to ischemia or hypoglycemia is CA1 hippocampal region due to pyramidal neurons death. Glutamate receptors are involved together with protein-kinase C and nitric oxide synthase. Long-term potentiation (LTP) is generated in anoxic or hypoglycemic conditions via activation of NMDA while inhibition of these receptors attenuates this response. Protein-kinase C and nitric oxide synthase are involved in anoxic LTP mechanism. Postischemic neurons are hyperexcitable in CA3 area while CA1 pyramidal neurons degenerate and disappear. Changes of glutamate receptors triggered by ischemia and hypoglycemia are discussed in this review.
Animals↗