The role of cAMP in ethanol-regulated beta-endorphin release from hypothalamic neurons.
We have previously shown that ethanol acutely stimulates immunoreactive beta-endorphin (IR-beta-EP) release from hypothalamic neurons, whereas chronic administration of ethanol desensitizes these neurons. In the study reported herein, the role of the intracellular cAMP system in the ethanol-regulated IR-beta-EP release from hypothalamic cells in primary cultures was investigated. Acute treatment with ethanol or with the cAMP analog, dibutyryl cAMP, revealed that both agents stimulate the release of IR-beta-EP from the hypothalamic cells. Combined treatment of ethanol and the cAMP analog produced a synergistic effect on IR-beta-EP release. Treatment with ethanol and a cAMP-elevating agent, forskolin, increased cAMP levels in cultured hypothalamic cells. However, prior exposure to ethanol reduced the cAMP-elevating responses of these neurons to ethanol and forskolin. These results indicate that the stimulatory and adaptive responses of IR-beta-EP neurons to ethanol may involve the cAMP system.
Boyadjieva
N I
NI
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman 99164-6520, USA.
Sarkar
D K
DK
D000818:Animals; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000502:physiology*; D000431:Ethanol / Q000494:pharmacology*; D005333:Fetus; D007031:Hypothalamus / Q000187:drug effects* / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D001615:beta-Endorphin / Q000378:metabolism*
D000431:Ethanol; D001615:beta-Endorphin; D000242:Cyclic AMP