Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous arginine vasopressin was previously shown to modulate the rate of loss of functional (CNS) tolerance to ethanol, suggesting that chronic ethanol ingestion might alter vasopressin synthesis and/or release. Since extrahypothalamic vasopressin is believed to be involved in the CNS effects of the peptide, we determined the effect of ethanol on vasopressin mRNA in the bed nucleus of the stria terminalis (BST), as well as in several hypothalamic nuclei. Chronic ethanol ingestion, that produced functional tolerance and physical dependence in mice, resulted in decreased vasopressin mRNA levels in all areas examined. In contrast, as expected, dehydration resulted in increases in vasopressin mRNA in the BST and in all hypothalamic nuclei except the suprachiasmatic nucleus. In the BST, both ethanol ingestion and dehydration affected cells in the central region of the nucleus, while cells in the caudal portion were only affected by ethanol treatment. The results indicate that chronic ethanol ingestion generally reduces the synthesis of vasopressin, and that increased vasopressin synthesis is not necessary in order for the peptide to affect ethanol tolerance.
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PMID:Chronic ethanol ingestion decreases vasopressin mRNA in hypothalamic and extrahypothalamic nuclei of mouse brain. 174 46

Among the many factors that may influence the development or expression of functional tolerance to or physical dependence on ethanol is the neurohypophyseal hormone, arginine vasopressin (AVP). This peptide hormone, administered exogenously, maintains ethanol tolerance in animals once such tolerance has been established. An analog of the hormone has also been reported to facilitate the development of ethanol tolerance and to exacerbate ethanol withdrawal symptomatology. Neurohypophyseal hormones and structurally related peptides have previously been shown to influence learning or memory; however, structure-activity analyses reveal differences in the structural requirements for maintenance of ethanol tolerance as compared to facilitation of memory processes. Therefore, these phenomena may represent CNS adaptive processes which are subserved by different mechanisms, or are differentially sensitive to particular peptides. The initial sensitivity of an animal to ethanol can also be affected by peptides, notably thyrotropin releasing hormone (thyroliberin, TRH). TRH antagonizes many of the initial responses to ethanol, perhaps by non-specific means. AVP, however, appears to potentiate the sedative effect of an acute dose of ethanol. Neurohypophyseal peptides also modulate ethanol intake. Thus, these neuropeptides, which have been localized to many areas of brain, may serve as endogenous modulators of various parameters related to ethanol consumption.
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PMID:Centrally acting peptides and tolerance to ethanol. 612 10