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.
Key Words
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Article info
Publication history
Published online: February 22, 2011
Accepted:
December 29,
2010
Received in revised form:
December 29,
2010
Received:
June 10,
2010
Footnotes
Authors WPN and TLK contributed equally to this work.
Identification
Copyright
© 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.