Time course of development of supersensitivity to topical acetylcholine in partially isolated cortex.
In alert monkeys the time course for development of supersensitivity to topical acetylcholine in partially isolated frontal cerebral cortex was determined. Thresholds for paroxysmal discharge fell progressively and markedly during 3 weeks, further in 5 and somewhat more after 6 months. ACh supersensitivity was demonstrated in chronic "isolated" occipital cortex. Epileptiform discharges were recorded selectively from chronic partially isolated frontal cortex on peripheral nerve stimulation and these spread, causing a clinical convulsive siezure when the open end of the isolation extended into the precentral gyrus. The basic mechanisms responsible for the supersensitivity are unknown but evidence presented and much in the pertinent literature is in keeping with the hypothesis that partial isolation of cortical cells, i.e., denervation, deafferentation, or disuse may be important. It is suggrested that peripheral nerve stimulation, like arousal, may cause an outflow of ACh on the normal brain surface and over the open end of a partially isolated area, which, especially, in the presence of a diminished cholinesterase activity (in partially isolated cortex), could act like topical ACh, cause a DC shift and an epileptiform discharge.
D000109:Acetylcholine / Q000494:pharmacology*; D000287:Administration, Topical; D000818:Animals; D003714:Denervation; D004558:Electric Stimulation; D004569:Electroencephalography; D005625:Frontal Lobe / Q000187:drug effects*; D008251:Macaca; D009778:Occipital Lobe / Q000187:drug effects; D012640:Seizures / Q000139:chemically induced; D013997:Time Factors
D000109:Acetylcholine