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000857102 1001_ $$00000-0002-5702-1342$$aHarris, Nicholas A.$$b0
000857102 245__ $$aDorsal BNST α 2A -Adrenergic Receptors Produce HCN-Dependent Excitatory Actions That Initiate Anxiogenic Behaviors
000857102 260__ $$aWashington, DC$$bSoc.69657$$c2018
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000857102 520__ $$aStress is a precipitating agent in neuropsychiatric disease and initiates relapse to drug-seeking behavior in addicted patients. Targeting the stress system in protracted abstinence from drugs of abuse with anxiolytics may be an effective treatment modality for substance use disorders. α2A-adrenergic receptors (α2A-ARs) in extended amygdala structures play key roles in dampening stress responses. Contrary to early thinking, α2A-ARs are expressed at non-noradrenergic sites in the brain. These non-noradrenergic α2A-ARs play important roles in stress responses, but their cellular mechanisms of action are unclear. In humans, the α2A-AR agonist guanfacine reduces overall craving and uncouples craving from stress, yet minimally affects relapse, potentially due to competing actions in the brain. Here, we show that heteroceptor α2A-ARs postsynaptically enhance dorsal bed nucleus of the stria terminalis (dBNST) neuronal activity in mice of both sexes. This effect is mediated by hyperpolarization-activated cyclic nucleotide-gated cation channels because inhibition of these channels is necessary and sufficient for excitatory actions. Finally, this excitatory action is mimicked by clozapine-N-oxide activation of the Gi-coupled DREADD hM4Di in dBNST neurons and its activation elicits anxiety-like behavior in the elevated plus maze. Together, these data provide a framework for elucidating cell-specific actions of GPCR signaling and provide a potential mechanism whereby competing anxiogenic and anxiolytic actions of guanfacine may affect its clinical utility in the treatment of addiction.
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000857102 7001_ $$00000-0003-1306-4196$$aIsaac, Austin T.$$b1
000857102 7001_ $$00000-0001-8081-9275$$aGünther, Anne$$b2
000857102 7001_ $$0P:(DE-HGF)0$$aMerkel, Kevin$$b3
000857102 7001_ $$00000-0002-0223-077X$$aMelchior, James$$b4
000857102 7001_ $$0P:(DE-HGF)0$$aXu, Michelle$$b5
000857102 7001_ $$0P:(DE-HGF)0$$aEguakun, Eghosa$$b6
000857102 7001_ $$00000-0001-7788-4631$$aPerez, Rafael$$b7
000857102 7001_ $$00000-0001-9459-2462$$aNabit, Brett P.$$b8
000857102 7001_ $$0P:(DE-HGF)0$$aFlavin, Stephanie$$b9
000857102 7001_ $$00000-0002-0895-1535$$aGilsbach, Ralf$$b10
000857102 7001_ $$0P:(DE-HGF)0$$aShonesy, Brian$$b11
000857102 7001_ $$00000-0003-1297-0007$$aHein, Lutz$$b12
000857102 7001_ $$00000-0003-2423-4592$$aAbel, Ted$$b13
000857102 7001_ $$0P:(DE-Juel1)131911$$aBaumann, Arnd$$b14
000857102 7001_ $$00000-0002-1235-3802$$aMatthews, Robert$$b15
000857102 7001_ $$00000-0002-3941-7677$$aCentanni, Samuel W.$$b16
000857102 7001_ $$0P:(DE-HGF)0$$aWinder, Danny G.$$b17$$eCorresponding author
000857102 77318 $$2Crossref$$3journal-article$$a10.1523/jneurosci.0963-18.2018$$bSociety for Neuroscience$$d2018-08-27$$n42$$p8922-8942$$tThe Journal of Neuroscience$$v38$$x0270-6474$$y2018
000857102 773__ $$0PERI:(DE-600)1475274-8$$a10.1523/JNEUROSCI.0963-18.2018$$gVol. 38, no. 42, p. 8922 - 8942$$n42$$p8922-8942$$tThe journal of neuroscience$$v38$$x0270-6474$$y2018
000857102 8564_ $$uhttps://juser.fz-juelich.de/record/857102/files/8922.full.pdf$$yPublished on 2018-10-17. Available in OpenAccess from 2019-04-17.
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