Abstract
By micro-injecting carbachol or anticholinesterases changes were produced in the discharge patterns of hippocampal foci which had been established previously by induction with picrotoxin, D-tubocurarine or strychnine in acute cat preparations. Micro-injected carbachol, an acetylcholine analog, excited the foci, which exhibited a markedly accelerated firing rate, lengthened after-discharge duration, and frequent intervals of intermittent seizure discharges. These excitatory actions were readily reversed by local scopolamine. Of the anticholinesterases, lipid-soluble physostigmine and diisopropyl fluorophosphate initially increased firing rates without significantly altering after-discharge; subsequently, both anti-cholinesterases stabilized the foci, reducing or completely eliminating the after-discharge component. Significantly, the after-discharge was restored with small supplemental micro-injection of acetylcholine at the site. Lipid-insoluble neostigmine, although an anticholinesterase, caused exitatory effects on foci similar to those of carbachol, to which it bears some chemical resemblance. Effectiveness of scopolamine in abolishing the after-discharge component suggests a cholinergic link in the phenomenon of focogenesis in the hippocampus. Increased cholinergic activity can involve two local cholinoceptive mechanisms which can influence hippocampal foci differentially. One of these, superficial and readily accessible, excites the focus and leads to seizure discharges; the other, interior and limited by a lipid diffusional barrier, reduces excitability and stabilizes the focus. The excitatory mechanism, however, can supersede the inhibitory one. The critical regulatory role of these cholinoceptive mechanisms in influencing the activities of hippocampal foci is emphasized throughout the study.
Published Version
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