Chunk #109 — 3 Neuropeptide Roles in Acute and Chronic Alcohol Actions — 3.1 Corticotropin-Releasing Factor — 3.1.3 Corticotropin-Releasing Factor Actions in the Bed Nucleus of the Stria Terminalis
Francesconi et al. (2009a, b) investigated the effects of protracted withdrawal from alcohol in the juxtacapsular nucleus of the anterior division of the BNST (jcBNST). The jcBNST receives robust glutamatergic projections from the Basolateral amygdal (BLA), the postpiriform transition area, and the insular cortex as well as dopamine inputs from the midbrain. In turn, the jcBNST sends GABAergic projections to the medial division of the central nucleus of the amygdala (CeAm) as well as other brain regions. These investigators described a form of long-term potentiation of the intrinsic excitability (LTP-IE) of neurons of the jcBNST in response to high-frequency stimulation (HFS) of the stria terminalis that was impaired during protracted withdrawal from alcohol (Francesconi et al. 2009b). Administration of the selective CRF1R antagonist (R121919), but not of the CRF2R antagonist (astressin 2B), normalized jcBNST LTP-IE in animals with a history of alcohol dependence (Francesconi et al. 2009b). In addition, repeated, but not acute, administration of CRF itself produced a decreased jcBNST LTP-IE. These investigators also showed that dopaminergic neurotransmission is required for the induction of LTP-IE of jcBNST neurons through
