title: Rapid synapse-specific regulation of hypothalamic magnocellular neurons by glucocorticoids.
abstract: Glucocorticoids secreted in response to stress activation of the hypothalamic-pituitary-adrenal axis feed back onto the hypothalamus to rapidly suppress neuroendocrine activation, including oxytocin and vasopressin secretion. Here we provide a brief review focused on our recent findings of a rapid glucocorticoid-induced opposing regulation of glutamate and gamma-aminobutyric acid (GABA) inputs to magnocellular neurons via the release of distinct retrograde messengers. The stress hormone corticosterone and its synthetic analogue dexamethasone elicit the rapid retrograde release of endocannabinoids by activating a novel membrane-associated, G protein-coupled receptor in parvocellular and magnocellular neuroendocrine cells of the hypothalamic paraventricular and supraoptic nuclei. Glucocorticoids also cause the rapid retrograde release of an unknown messenger that facilitates presynaptic GABA release onto magnocellular neuroendocrine cells. These finding suggest that there is a strict synapse-specific segregation of the opposing actions of the two retrogradely released messengers. Thus, the combined actions of glucocorticoids cause a rapid synaptic inhibition of the magnocellular neurons and would be expected, therefore, to mediate a rapid feedback inhibition of the secretion of oxytocin and vasopressin during stress activation of the hypothalamic-pituitary-adrenal axis.
authors.affiliation: Neurobiology Division, Department of Cell and Molecular Biology, Tulane University, New Orleans, LA, USA.
authors.forename: Shi
authors.initials: S
authors.lastname: Di
authors.forename: Jeffrey G
authors.initials: JG
authors.lastname: Tasker
mesh_terms: D000818:Animals; D020532:Basal Nucleus of Meynert / Q000502:physiology*; D003907:Dexamethasone / Q000494:pharmacology*; D025461:Feedback, Physiological / Q000187:drug effects / Q000502:physiology; D005938:Glucocorticoids / Q000494:pharmacology*; D018698:Glutamic Acid / Q000502:physiology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology; D008322:Mammals; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology; D015290:Second Messenger Systems / Q000187:drug effects / Q000502:physiology; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D050916:TRPV Cation Channels / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000502:physiology
chemical_list: D005938:Glucocorticoids; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D003907:Dexamethasone; D009638:Norepinephrine