Evidence that central nicotinic-acetylcholine receptors are involved in the modulation of basal and stress-induced adrenocortical responses.
We investigated the involvement of central nervous system nicotinic-acetylcholine receptors in the secretory activity of the hypothalamic-hypophyseal-adrenal axis. Antiacetylcholine receptor antibodies derived from rabbits immunized with purified Torpedo-acetylcholine receptor or from myasthenia gravis patients were injected intracerebroventricularly into adult male rats for 5 consecutive days. Treatment with both preparations caused increased basal corticosterone concentrations, inhibition of the corticosterone response to ether stress, and neurological signs and motor dysfunctions. The adrenocortical response in experimental autoimmune myasthenia gravis Lewis rats with high circulating antiacetylcholine receptor antibodies was also tested. These rats exhibited a marked increase in basal corticosterone concentrations and a normal response to ether stress. The results showed that antinicotinic-acetylcholine receptor antibodies, either circulating or intraventricularly administered, can modulate both basal and stress-induced adrenocortical secretion.
D000302:Adrenal Cortex / Q000378:metabolism; D000818:Animals; D000906:Antibodies / Q000502:physiology*; D001831:Body Temperature; D001835:Body Weight; D003345:Corticosterone / Q000097:blood*; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D007276:Injections, Intraventricular; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009157:Myasthenia Gravis / Q000097:blood* / Q000276:immunology; D051381:Rats; D011917:Rats, Inbred Lew; D011978:Receptors, Nicotinic / Q000276:immunology / Q000502:physiology*; D013312:Stress, Physiological / Q000097:blood*
D000906:Antibodies; D011978:Receptors, Nicotinic; D003345:Corticosterone