Muscarinic cholinergic regulation of epileptic spiking in kindling

J. Gregory Fitz, James O. McNamara

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Electroencephalographic monitoring of spontaneous interictal spiking (SIS) following kindling demonstrated that SIS occurs in both amygdalas and that it declines sharply during the pays following kindling. Systemically administered muscarinic antagonists which pass the blood-brain barrier (atropine and scopolamine) activated interictal spiking in kindled rats but not in controls. Interictal spiking activated by atropine was reversed by physostigmine. Both physostigmine and choline, agents which increase brain ACh concentration by different mechanisms, caused a reduction in spontaneous (not drug activated) interictal spiking. The results of these pharmacologic studies indicate that the interaction of endogenous ACh with central muscarinic receptors is capable of suppressing SIS in kindled rats. Whether cholinergic suppression of SIS represents a convulsant or an anticonvulsant action is presently unclear.

Original languageEnglish (US)
Pages (from-to)117-127
Number of pages11
JournalBrain Research
Volume178
Issue number1
DOIs
StatePublished - Dec 7 1979

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Fingerprint Dive into the research topics of 'Muscarinic cholinergic regulation of epileptic spiking in kindling'. Together they form a unique fingerprint.

  • Cite this