Antagonism of central but not peripheral cholinergic receptors retards amygdala kindling in rats

• Published in: Experimental neurology Vol. 95; no. 1; pp. 194 - 206
• Main Authors: Westerberg, Verner, Corcoran, Michael E
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 1987; Elsevier
• Subjects: Amygdala - physiology; Animals; Anticonvulsants; Biological and medical sciences; Brain - drug effects; Kindling, Neurologic - drug effects; Male; Medical sciences; Membrane Potentials - drug effects; N-Methylscopolamine; Nervous system involvement in other diseases. Miscellaneous; Neurology; Rats; Rats, Inbred Strains; Receptors, Cholinergic - drug effects; Scopolamine - pharmacology; Scopolamine Derivatives - pharmacology; AD; Peripheral nervous system; Experimental disease; Cholinergic receptor; Nervous system diseases; Epilepsy; Central nervous system; Antagonist; Amygdaloid nucleus
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/0014-4886(87)90017-3

The effects of antagonism of muscarinic cholinergic receptors on the development of seizures produced by electrical stimulation of the amygdala (kindling) were assessed in three experiments. Rats pretreated with the muscarinic antagonist scopolamine developed seizures more slowly than did untreated rats. Whereas scopolamine retarded the development of seizures in a dose-dependent manner, it did not affect the intensity or duration of seizures when administered to kindled control rats. Pretreatment with methyl scopolamine, a quaternary derivative of scopolamine that does not readily cross the blood-brain barrier, did not affect the rate of development of seizures, nor did it affect established seizures. Thus the prophylactic effects of scopolamine are produced in the central nervous system and not in the periphery. The results from these experiments are consistent with the idea that central cholinergic or cholinoceptive neurons are critically involved in amygdala kindling.