β-Adrenergic receptors enhance excitatory transmission in the bed nucleus of the stria terminalis through a corticotrophin-releasing factor receptor dependent and cocaine-regulated mechanism

William P. Nobis, Thomas L. Kash, Yuval Silberman, Danny G. Winder

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

Background: Evidence suggests that the noradrenergic and corticotrophin-releasing factor (CRF) systems play critical roles in relapse and stress-related behaviors. In particular, behavioral studies point to a serial signaling process initiated by β-adrenergic receptors that requires CRF receptor (CRFR)-dependent signaling in the bed nucleus of the stria terminalis (BNST) to produce stress-induced relapse to cocaine seeking. Methods: We used whole cell patch clamp recordings from acutely prepared mouse brain slices to examine the actions of β-adrenergic receptors and CRFR1 on excitatory transmission in BNST. We examined the effects of agonists of these receptors in slices prepared from naive, sham, and cocaine-conditioned mice. Results: β1-adrenergic receptor activation within the BNST produces an enhancement of excitatory synaptic transmission that requires CRFR1-dependent signaling. We show that chronic cocaine administration transiently disrupts β1-adrenergic- and CRFR1-dependent enhancement of glutamatergic transmission, that this disruption wanes with time, and that it can be reintroduced with a cocaine challenge. Conclusions: In total, these studies identify a circuit mechanism within the BNST that may play an important role in CRF- and norepinephrine-regulated behaviors.

Original languageEnglish (US)
Pages (from-to)1083-1090
Number of pages8
JournalBiological Psychiatry
Volume69
Issue number11
DOIs
StatePublished - Jun 1 2011

All Science Journal Classification (ASJC) codes

  • Biological Psychiatry

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