Cholinergic activation of the electrocorticogram: Role of the substantia innominata and effects of atropine and quinuclidinyl benzilate
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Systemic injection of quinuclidinyl benzilate partially abolished low voltage fast activity (LVFA) in the neocortex of waking rats, resulting in the appearance of large irregular slow waves during Type 2 behaviors (e.g. immobility, sniffing without head movement, face washing). These slow waves did not occur during Type 1 behavior (e.g. walking, head movement). Atropine sulfate produced a similar effect but it was less potent by a factor of about 12. Injection of kainic acid into the substantia innominata: (a) destroyed local cells which contain acetylcholinesterase (AChE) and reduced AChE staining in the ipsilateral neocortex; and (b) produced large slow waves in the ipsilateral neocortex during Type 2 behavior but not during Type 1 behavior. These slow waves were abolished by systemic injection of pilocarpine. Kainic acid injection into the thalamus produced extensive local cell loss but failed to produce slow waves in the neocortex. The data suggest that the LVFA which is normally present in the neocortex during waking Type 2 behavior is dependent on a cholinergic input to the neocortex from the substantia innominata. The relevance of these findings to Alzheimer's disease is discussed.
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