Serotonin and Electroconvulsive Shock-Induced Prolactin Release.
Conrad M. Swartz, Richard Abrams, Victoria Drews
Abstract
Conrad M. Swartz, Richard Abrams, Victoria Drews
Abstract
Baseline and post-electroconvulsive shock (ECS) prolactin levels were determined in serum samples from 13 rabbits, with and without pretreatment with the serotonin-2 (5-HT(2)) receptor blocker ketanserin. Without ketanserin, ECS did not raise serum prolactin levels over baseline. After ketanserin, baseline serum prolactin levels were 50% lower and post-ECS prolactin levels were twice this new baseline level and close to post-ECS prolactin levels without ketanserin. These observations suggest that serotonergic neurotransmission potentiates stress-induced prolactin secretion, but contributes little to ECS-induced prolactin release.
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Baseline and post-electroconvulsive shock (ECS) prolactin levels were determined in serum samples from 13 rabbits, with and without pretreatment with the serotonin-2 (5-HT(2)) receptor blocker ketanserin. Without ketanserin, ECS did not raise serum prolactin levels over baseline. After ketanserin, baseline serum prolactin levels were 50% lower and post-ECS prolactin levels were twice this new baseline level and close to post-ECS prolactin levels without ketanserin. These observations suggest that serotonergic neurotransmission potentiates stress-induced prolactin secretion, but contributes little to ECS-induced prolactin release.
Key concepts: Prolactin, Ketanserin, Serotonergic, Internal medicine, Endocrinology, Serotonin, Medicine, Receptor