Chunk #103 — 3 Neuropeptide Roles in Acute and Chronic Alcohol Actions — 3.1 Corticotropin-Releasing Factor — 3.1.2 Corticotropin-Releasing Factor Actions in the Central Amygdala
the frequency of GABAR-mediated mIPSCs, and this effect is blocked by CRF1R antagonists (Nie et al. 2004; 2009; Roberto et al. 2010). Thus, EtOH probably enhances the release of GABA by activating CRF1R on GABAergic terminals (Nie et al. 2009; Roberto et al. 2010). Conversely, CRF1R antagonists directly increased PPF of IPSCs and decreased mIPSC frequencies, consistent with decreased GABA release, thus opposing EtOH effects. Because GABA and CRF are often co-localized in CeA neurons, the EtOH-elicited GABA release may involve release of the CRF peptide itself, perhaps even from the terminals synapsing on autoreceptors on the same cell bodies or on collaterals from other GABAergic interneurons. Thus, this example raises the possibility of involvement of other, secondary messengers in EtOH effects on GABAergic terminals.
