Journal
BIOLOGICAL PSYCHIATRY
Volume 69, Issue 11, Pages 1083-1090Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2010.12.030
Keywords
Addiction; beta adrenergic; cocaine; corticotrophin-releasing factor (CRF); glutamate; norepinephrine
Categories
Funding
- National Institute on Alcohol Abuse and Alcoholism
- National Institute on Drug Abuse
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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 beta-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 beta-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: beta(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 beta(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.
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