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.

Nobis WP, Kash TL, Silberman Y, Winder DG
Biol Psychiatry. 2011 69 (11): 1083-90

PMID: 21334600 · PMCID: PMC3090515 · DOI:10.1016/j.biopsych.2010.12.030

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.

Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

MeSH Terms (14)

Animals Cocaine Corticotropin-Releasing Hormone Dopamine Uptake Inhibitors Glutamic Acid Male Mice Mice, Inbred C57BL Neurons Patch-Clamp Techniques Receptors, Adrenergic, beta Receptors, Corticotropin-Releasing Hormone Septal Nuclei Synaptic Transmission

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