Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons
Autor(a) principal: | |
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Data de Publicação: | 2005 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UCB |
Texto Completo: | http://twingo.ucb.br:8080/jspui/handle/10869/517 https://repositorio.ucb.br:9443/jspui/handle/123456789/7769 |
Resumo: | Glucocorticoids secreted in response to stress activation of the hypothalamic-pituitary-adrenal axis feed back onto the brain to rapidly suppress neuroendocrine activation, including oxytocin and vasopressin secretion. Here we show using whole-cell patch clamp recordings that glucocorticoids elicit a rapid, opposing action on synaptic glutamate and -aminobutyric acid (GABA) release onto magnocellular neurons of the hypothalamic supraoptic nucleus and paraventricular nucleus, suppressing glutamate release and facilitating GABA release by activating a putative membrane receptor. The glucocorticoid effect on both glutamate and GABA release was blocked by inhibiting postsynaptic G protein activity, suggesting a dependence on postsynaptic G protein signaling and the involvement of a retrograde messenger. Biochemical analysis of hypothalamic slices treated with dexamethasone revealed a glucocorticoid-induced rapid increase in the levels of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The glucocorticoid suppression of glutamate release was blocked by the type I cannabinoid receptor cannabinoid receptor antagonist, AM251, and was mimicked and occluded by AEA and 2-AG, suggesting it was mediated by retrograde endocannabinoid release. The glucocorticoid facilitation of GABA release was also blocked by AM251 but was not mimicked by AEA, 2-AG, or a synthetic cannabinoid, WIN 55,2122, nor was it blocked by vanilloid or ionotropic glutamate receptor antagonists, suggesting that it was mediated by a retrograde messenger acting at an AM251-sensitive, noncannabinoid/nonvanilloid receptor at presynaptic GABA terminals. The combined, opposing actions of glucocorticoids mediate a rapid inhibition of the magnocellular neuroendocrine cells, which in turn should mediate rapid feedback inhibition of the secretion of oxytocin and vasopressin by glucocorticoids during stress activation of the hypothalamic-pituitary-adrenal axis. |
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Shi DiMalcher-Lopes, RenatoMarcheselli, Victor L.Bazan, Nicolas G.Tasker, Jeffrey G.2016-10-10T03:52:36Z2016-10-10T03:52:36Z2005SHI DI et al. Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons. Endocrinology, v.145, n.10, p. 4292–4301, 2005.http://twingo.ucb.br:8080/jspui/handle/10869/517https://repositorio.ucb.br:9443/jspui/handle/123456789/7769Glucocorticoids secreted in response to stress activation of the hypothalamic-pituitary-adrenal axis feed back onto the brain to rapidly suppress neuroendocrine activation, including oxytocin and vasopressin secretion. Here we show using whole-cell patch clamp recordings that glucocorticoids elicit a rapid, opposing action on synaptic glutamate and -aminobutyric acid (GABA) release onto magnocellular neurons of the hypothalamic supraoptic nucleus and paraventricular nucleus, suppressing glutamate release and facilitating GABA release by activating a putative membrane receptor. The glucocorticoid effect on both glutamate and GABA release was blocked by inhibiting postsynaptic G protein activity, suggesting a dependence on postsynaptic G protein signaling and the involvement of a retrograde messenger. Biochemical analysis of hypothalamic slices treated with dexamethasone revealed a glucocorticoid-induced rapid increase in the levels of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The glucocorticoid suppression of glutamate release was blocked by the type I cannabinoid receptor cannabinoid receptor antagonist, AM251, and was mimicked and occluded by AEA and 2-AG, suggesting it was mediated by retrograde endocannabinoid release. The glucocorticoid facilitation of GABA release was also blocked by AM251 but was not mimicked by AEA, 2-AG, or a synthetic cannabinoid, WIN 55,2122, nor was it blocked by vanilloid or ionotropic glutamate receptor antagonists, suggesting that it was mediated by a retrograde messenger acting at an AM251-sensitive, noncannabinoid/nonvanilloid receptor at presynaptic GABA terminals. The combined, opposing actions of glucocorticoids mediate a rapid inhibition of the magnocellular neuroendocrine cells, which in turn should mediate rapid feedback inhibition of the secretion of oxytocin and vasopressin by glucocorticoids during stress activation of the hypothalamic-pituitary-adrenal axis.Made available in DSpace on 2016-10-10T03:52:36Z (GMT). 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dc.title.pt_BR.fl_str_mv |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
title |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
spellingShingle |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons Shi Di |
title_short |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
title_full |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
title_fullStr |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
title_full_unstemmed |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
title_sort |
Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons |
author |
Shi Di |
author_facet |
Shi Di Malcher-Lopes, Renato Marcheselli, Victor L. Bazan, Nicolas G. Tasker, Jeffrey G. |
author_role |
author |
author2 |
Malcher-Lopes, Renato Marcheselli, Victor L. Bazan, Nicolas G. Tasker, Jeffrey G. |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Shi Di Malcher-Lopes, Renato Marcheselli, Victor L. Bazan, Nicolas G. Tasker, Jeffrey G. |
dc.description.abstract.por.fl_txt_mv |
Glucocorticoids secreted in response to stress activation of the hypothalamic-pituitary-adrenal axis feed back onto the brain to rapidly suppress neuroendocrine activation, including oxytocin and vasopressin secretion. Here we show using whole-cell patch clamp recordings that glucocorticoids elicit a rapid, opposing action on synaptic glutamate and -aminobutyric acid (GABA) release onto magnocellular neurons of the hypothalamic supraoptic nucleus and paraventricular nucleus, suppressing glutamate release and facilitating GABA release by activating a putative membrane receptor. The glucocorticoid effect on both glutamate and GABA release was blocked by inhibiting postsynaptic G protein activity, suggesting a dependence on postsynaptic G protein signaling and the involvement of a retrograde messenger. Biochemical analysis of hypothalamic slices treated with dexamethasone revealed a glucocorticoid-induced rapid increase in the levels of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The glucocorticoid suppression of glutamate release was blocked by the type I cannabinoid receptor cannabinoid receptor antagonist, AM251, and was mimicked and occluded by AEA and 2-AG, suggesting it was mediated by retrograde endocannabinoid release. The glucocorticoid facilitation of GABA release was also blocked by AM251 but was not mimicked by AEA, 2-AG, or a synthetic cannabinoid, WIN 55,2122, nor was it blocked by vanilloid or ionotropic glutamate receptor antagonists, suggesting that it was mediated by a retrograde messenger acting at an AM251-sensitive, noncannabinoid/nonvanilloid receptor at presynaptic GABA terminals. The combined, opposing actions of glucocorticoids mediate a rapid inhibition of the magnocellular neuroendocrine cells, which in turn should mediate rapid feedback inhibition of the secretion of oxytocin and vasopressin by glucocorticoids during stress activation of the hypothalamic-pituitary-adrenal axis. |
dc.description.version.pt_BR.fl_txt_mv |
Sim |
dc.description.status.pt_BR.fl_txt_mv |
Publicado |
description |
Glucocorticoids secreted in response to stress activation of the hypothalamic-pituitary-adrenal axis feed back onto the brain to rapidly suppress neuroendocrine activation, including oxytocin and vasopressin secretion. Here we show using whole-cell patch clamp recordings that glucocorticoids elicit a rapid, opposing action on synaptic glutamate and -aminobutyric acid (GABA) release onto magnocellular neurons of the hypothalamic supraoptic nucleus and paraventricular nucleus, suppressing glutamate release and facilitating GABA release by activating a putative membrane receptor. The glucocorticoid effect on both glutamate and GABA release was blocked by inhibiting postsynaptic G protein activity, suggesting a dependence on postsynaptic G protein signaling and the involvement of a retrograde messenger. Biochemical analysis of hypothalamic slices treated with dexamethasone revealed a glucocorticoid-induced rapid increase in the levels of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG). The glucocorticoid suppression of glutamate release was blocked by the type I cannabinoid receptor cannabinoid receptor antagonist, AM251, and was mimicked and occluded by AEA and 2-AG, suggesting it was mediated by retrograde endocannabinoid release. The glucocorticoid facilitation of GABA release was also blocked by AM251 but was not mimicked by AEA, 2-AG, or a synthetic cannabinoid, WIN 55,2122, nor was it blocked by vanilloid or ionotropic glutamate receptor antagonists, suggesting that it was mediated by a retrograde messenger acting at an AM251-sensitive, noncannabinoid/nonvanilloid receptor at presynaptic GABA terminals. The combined, opposing actions of glucocorticoids mediate a rapid inhibition of the magnocellular neuroendocrine cells, which in turn should mediate rapid feedback inhibition of the secretion of oxytocin and vasopressin by glucocorticoids during stress activation of the hypothalamic-pituitary-adrenal axis. |
publishDate |
2005 |
dc.date.issued.fl_str_mv |
2005 |
dc.date.accessioned.fl_str_mv |
2016-10-10T03:52:36Z |
dc.date.available.fl_str_mv |
2016-10-10T03:52:36Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/article |
status_str |
publishedVersion |
format |
article |
dc.identifier.citation.fl_str_mv |
SHI DI et al. Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons. Endocrinology, v.145, n.10, p. 4292–4301, 2005. |
dc.identifier.uri.fl_str_mv |
http://twingo.ucb.br:8080/jspui/handle/10869/517 https://repositorio.ucb.br:9443/jspui/handle/123456789/7769 |
identifier_str_mv |
SHI DI et al. Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of Glutamate and y-aminobutyric acid Inputs to hypothalamic magnocellular neurons. Endocrinology, v.145, n.10, p. 4292–4301, 2005. |
url |
http://twingo.ucb.br:8080/jspui/handle/10869/517 https://repositorio.ucb.br:9443/jspui/handle/123456789/7769 |
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eng |
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eng |
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openAccess |
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