Chunk #102 — 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
New electrophysiological data showed that CRF, like EtOH, also enhances GABAergic transmission in the rat CeA (Roberto et al. 2010). As in mice, CRF and EtOH actions involve presynaptic CRF1R activation at the CeA GABAergic synapses. Interestingly, the interactions between the CRF and GABAergic systems in the CeA may play an important role in alcohol reward and dependence (Roberto et al. 2010). These results suggest that the presynaptic effect of EtOH on GABA release in rodent CeA involves CRF1R and perhaps release of CRF itself. Thus, superfusion of CRF has an effect on GABA IPSCs equivalent to that of EtOH: an increase in IPSC amplitude of about 30–50%. Furthermore, both CRF and EtOH decreased PPF of IPSCs in mouse and rat neurons, and the effects of both were selectively blocked by CRF1R antagonists. In addition, both EtOH and CRF increase 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;
