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Both iso- and hyperosmotic ethanol stimulate release of hypothalamic thyrotropin-releasing hormone despite opposite effect on neuron volume
Previous studies have indicated that isosmolar, but not hyperosmolar, ethanol induces in vitro gonadotropin-releasing hormone secretion from the basal hypothalamus, presumably by causing cell swelling. Moreover, ethanol reduces secretion of another hypothalamic neuropeptide vasopressin. We have stud...
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Published in: | Neuroscience 1997-10, Vol.80 (4), p.1263-1269 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Previous studies have indicated that isosmolar, but not hyperosmolar, ethanol induces
in vitro gonadotropin-releasing hormone secretion from the basal hypothalamus, presumably by causing cell swelling. Moreover, ethanol reduces secretion of another hypothalamic neuropeptide vasopressin. We have studied the acute effect of ethanol on specific hypophysiotropic basal and K
+-stimulated thyrotropin-releasing hormone secretion
in vitro especially in relation to cell swelling. Isosmotic 40–160
mM ethanol increased thyrotropin-releasing hormone release from the hypothalamic paraventricular nucleus and median eminence in a dose-dependent manner. Both a 30% decrease of osmolarity and isosmotic 80
mM ethanol induced 12% swelling of hypothalamic neurons. Hyperosmotic 80
mM or 160
mM ethanol induced release of thyrotropin-releasing hormone from both hypothalamic structures but did not cause cell swelling (80
mM) or even induced cell shrinkage (160
mM). Depletion of medium Ca
2+ did not affect thyrotropin-releasing hormone secretion caused by either isosmotic or hyperosmotic ethanol.
Our data indicate that both iso- and hyperosmotic ethanol stimulated release of hypophysiotropic thyrotropin-releasing hormone despite opposite effects on neuron volume. The mechanism of ethanol action appears complex and variable depending on the type of cell and neuropeptide affected. |
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ISSN: | 0306-4522 1873-7544 |
DOI: | 10.1016/S0306-4522(97)00176-0 |