Changes in the strength of recurrent inhibition in cobalt-induced epilepsy.
Changes in the strength of recurrent inhibition in the feline cortex in cobalt (CoCl2)-induced epilepsy were observed. The strength of inhibition was analyzed in terms of paired-pulse depression of the amplitude of somatosensory evoked potentials (SEPs) elicited by stimulation of the ventral posterolateral (VPL) thalamic nucleus. An enhancement in recurrent inhibition was observed shortly after CoCl2 application. The size of the amplitude of cortical evoked potentials (EPs) elicited by VPL stimulation increased simultaneously. The reduction of inhibition that appeared later was associated with afterdischarges (ADs) evoked by VPL stimulation. These ADs frequently extended to epileptic discharges. These results suggest that the reduction in recurrent inhibition induced by CoCl2 application plays an important role in the spread of seizure activity.
Kawakami
Y
Y
Department of Physiology, Tokyo Women's Medical College, Japan.
Koyama
I
I
D000818:Animals; D002415:Cats; D003035:Cobalt / Q000008:administration & dosage / Q000494:pharmacology; D004195:Disease Models, Animal; D004569:Electroencephalography; D004828:Epilepsies, Partial / Q000139:chemically induced* / Q000503:physiopathology; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects* / Q000502:physiology; D013787:Thalamic Nuclei / Q000187:drug effects / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D003035:Cobalt; D005680:gamma-Aminobutyric Acid; C018021:cobaltous chloride