Alteration in dentate neuronal activities associated with perforant path kindling: II. Decrease in granule cell excitability

Changes in the excitability of the dentate granule cells after perforant path kindling were examined by the analysis of perforant path-dentate gyrus field potentials recorded in freely moving rats. Using a range of test pulse intensities, the population spike heights (cellular output) were plotted a...

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Veröffentlicht in:Experimental neurology 1987, Vol.96 (1), p.33-45
Hauptverfasser: Maru, Eiichi, Goddard, Graham V.
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Sprache:eng
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Zusammenfassung:Changes in the excitability of the dentate granule cells after perforant path kindling were examined by the analysis of perforant path-dentate gyrus field potentials recorded in freely moving rats. Using a range of test pulse intensities, the population spike heights (cellular output) were plotted against the magnitudes of the associated population EPSPs (synaptic input), and a linear regression (input/output) was estimated from the relative linear portion of the plot. The χ-intercept of this regression defines the population spike threshold. With kindling, the overall amplitude of the population spikes decreased, in spite of an increase in the population EPSPs resulting in a flatter input/output regression. The χ-intercept of the regression was unaffected by the first kindling stimulation, but consistently and significantly increased with subsequent kindling. These changes gradually reverted to near the prekindling control values during a postkindling rest period of 1 moth, and were reinstated by rekindling after the period of rest. Similarly, the onset and peak latencies of the population spike were significantly retarded during the period of kindling. These results suggest that seizure activity causes a significant but temporary reduction in the excitability of dentate granule cells. This effect would tend to counteract the process of kindling and provide an explanation for some of the phenomena of postictal depression.
ISSN:0014-4886
1090-2430
DOI:10.1016/0014-4886(87)90166-X