% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Harris:857102,
author = {Harris, Nicholas A. and Isaac, Austin T. and Günther, Anne
and Merkel, Kevin and Melchior, James and Xu, Michelle and
Eguakun, Eghosa and Perez, Rafael and Nabit, Brett P. and
Flavin, Stephanie and Gilsbach, Ralf and Shonesy, Brian and
Hein, Lutz and Abel, Ted and Baumann, Arnd and Matthews,
Robert and Centanni, Samuel W. and Winder, Danny G.},
title = {{D}orsal {BNST} α 2{A} -{A}drenergic {R}eceptors {P}roduce
{HCN}-{D}ependent {E}xcitatory {A}ctions {T}hat {I}nitiate
{A}nxiogenic {B}ehaviors},
journal = {The journal of neuroscience},
volume = {38},
number = {42},
issn = {0270-6474},
address = {Washington, DC},
publisher = {Soc.69657},
reportid = {FZJ-2018-06356},
pages = {8922-8942},
year = {2018},
abstract = {Stress 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.},
cin = {ICS-4},
ddc = {610},
cid = {I:(DE-Juel1)ICS-4-20110106},
pnm = {552 - Engineering Cell Function (POF3-552)},
pid = {G:(DE-HGF)POF3-552},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30150361},
UT = {WOS:000447587500002},
doi = {10.1523/JNEUROSCI.0963-18.2018},
url = {https://juser.fz-juelich.de/record/857102},
}