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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.

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:β(1)-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 β(1)-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.

journal_name

Biol Psychiatry

journal_title

Biological psychiatry

authors

Nobis WP,Kash TL,Silberman Y,Winder DG

doi

10.1016/j.biopsych.2010.12.030

subject

Has Abstract

pub_date

2011-06-01 00:00:00

pages

1083-90

issue

11

eissn

0006-3223

issn

1873-2402

pii

S0006-3223(10)01362-4

journal_volume

69

pub_type

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