Chunk #108 — 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
In the same laboratory, a recent study showed the action of dopamine on cellular and synaptic function in the BNST. Kash et al. (2008) directly assessed the ability of dopamine to modulate neuronal function in the BNST using an ex vivo slice preparation. These investigators demonstrated a rapid and robust dopamine-induced enhancement of excitatory transmission in the BNST. This enhancement is activity-dependent and requires the downstream action of CRF1R, suggesting that dopamine induces CRF release through a local network mechanism. Furthermore, it was found that both in vivo and ex vivo cocaine induced a dopamine receptor and CRF1R-dependent enhancement of a form of NMDA receptor-dependent short-term potentiation in the BNST. These data highlight a direct and rapid interaction between dopamine and CRF systems that regulate excitatory transmission and plasticity in a brain region key to reinforcement and reinstatement. Because a rise in extracellular dopamine levels in the BNST is a shared consequence of multiple classes of drugs of abuse, this suggests that the CRF1R-dependent enhancement of glutamatergic transmission in this region may be a common key action of substances of abuse (Kash et al. 2008).
