Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuropeptide galanin (GAL) has been proposed to be an inhibitory modulator of cholinergic transmission in the hippocampus and may impair memory by directly affecting the activity of basal forebrain (BF) cholinergic neurons. Alternatively, GAL may act indirectly and modulate the activity of other neurotransmitter systems which, in turn, influence cholinergic transmission. We have used double in situ hybridization histochemistry to evaluate the co-expression of the GAL receptor subtype, GALR1, within cholinergic neurons in the medial septum/diagonal band of adult male rats. In alternate brain sections, we assessed the co-expression of GALR1 mRNA within another forebrain cell group implicated in memory functions, the neurons of the bed nucleus of the stria terminalis (BNST) and medial amygdala (AMe) which co-express vasopressin (VP) and GAL and project to septo-hippocampus. Despite the abundance of GALR1 mRNA-expressing neurons in the cholinergic BF, we found no evidence for the co-expression of this receptor subtype within cholinergic neurons in the medial septum/diagonal band. In contrast, we detected an extensive co-expression (95%) of GALR1 mRNA within extrahypothalamic VP/GAL neurons. These results do not support the idea that GAL, acting via the GALR1 receptor, directly impairs BF cholinergic neurons but suggest, instead, that non-cholinergic neurons in the BF may play a role in mediating the inhibitory actions of GAL on cholinergic function. However, our findings provide anatomical evidence that GAL could directly modulate the activity and/or secretion pattern of extrahypothalmic VP/GAL neurons into septo-hippocampal regions.
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PMID:GALR1 galanin receptor mRNA is co-expressed by galanin neurons but not cholinergic neurons in the rat basal forebrain. 945 Jun 84

Based on early immunocytochemical findings, galanin (GAL) was postulated to function as an inhibitory cotransmitter in rat cholinergic memory pathways. However, recent studies indicate that in the basal state GAL is not widely expressed by forebrain cholinergic neurons in rats. Inhibition of cholinergic transmission by cosecreted GAL may be enhanced under certain conditions, because GAL gene expression in the cholinergic basal forebrain is significantly increased prior to puberty and following nerve growth factor treatment. Other sources of GAL in rat septohippocampus that could interact with cholinergic pathways include noradrenergic neurons in the locus ceruleus and vasopressinergic neurons in the bed nucleus of the stria terminalis (BST) and medial amygdala (Me). GAL is extensively colocalized within these steroid-sensitive cell groups where its expression is upregulated by gonadal hormones. GAL, acting via the GALR1 receptor subtype, does not appear to directly regulate the activity of cholinergic neurons, but it may regulate the release of vasopressin and GAL into septohippocampus from BST/Me neurons.
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PMID:Regulation of galanin in memory pathways. 992 81

In golden hamsters, there is a complete absence of the small diameter vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BST) and medial amygdala (Me) which have been shown to exhibit steroid dependency and sexual dimorphism in many other rodent species. In rats, VP in the BST/Me is always colocalized with the neuropeptide galanin (GAL) and the sex difference in VP cell number appears to result from a sex difference in the number of GAL neurons which coexpress VP. Likewise, we reasoned that the species difference in extrahypothalamic VP pathways present in the golden hamster could result from a reduced coexpression of VP by GAL neurons in these regions. Here, we used in situ hybridization histochemistry to determine whether GAL mRNA expressing neurons are present in the BST and Me of golden hamsters despite the absence of VP expression in these regions. In addition, we have used slice binding and receptor autoradiography to identify specific GAL binding sites in the lateral septum, a probable target region of BST/Me neurons, and in situ hybridization to confirm that some of these binding sites correspond to the GALR1 GAL receptor subtype. Our findings indicate that the absence of VP expression in the BST/Me of golden hamsters results from a failure of extrahypothalamic GAL neurons to express the VP phenotype. Because GAL is expressed in the extended amygdaloid complex and GAL receptors are present in the septum of golden hamsters, GAL may play a role in modulating functions previously attributed to BST/Me pathways.
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PMID:Absence of vasopressin expression by galanin neurons in the golden hamster: implications for species differences in extrahypothalamic vasopressin pathways. 1010 Dec 29

Self-administration of ethanol and food share many common features and Richter hypothesized that an increase in ethanol consumption would decrease feeding to balance the excess calories contained in the ethanol. Previously, we have shown that individual alcohol consumption correlates with neurotransmitter gene expression, especially in the prefrontal cortex. To test the hypothesis of Richter, we measured hypothalamic gene expression of receptors or neuropeptides of known relevance for the regulation of food intake using qPCR and correlated this to individual ethanol consumption in Wistar rats. For validation, gene expression was first correlated with body weight. We found a correlation of dynorphin, somatostatin, melanocortin-4 receptor and serotonin 5-HT(2C) with body weight and trends to correlation for CART, thus confirming the established role of the hypothalamus in the regulation of weight. For ethanol consumption, correlations were found for CRH receptors 1 and 2 and vasopressin while strong trends were observed for galanin receptor 1, orexin receptor 1, MCH and adrenoceptor alpha(1B). Therefore, alcohol consumption does seem to involve several hypothalamic systems which also mediate feeding responses and suggests that the hypothalamus, together with the prefrontal cortex, may determine the 'stopping point' of an individual.
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PMID:The role of hypothalamic peptide gene expression in alcohol self-administration behavior. 1797 60