Ethanol produces corticotropin-releasing factor receptor-dependent enhancement of spontaneous glutamatergic transmission in the mouse central amygdala.
AUTHORS
Silberman
YYuval ,
Fetterly
TL Tracy L ,
Awad
EK Elias K ,
Milano
EJ Elana J ,
Usdin
TB Ted B ,
Winder
DG Danny G .
Alcoholism, clinical and experimental research. 2015 11 ; 39(11).
2154-62
- PMID: 26503065[PubMed].
- PMCID: PMC4624256.
- NIHMSID: NIHMS718132
ABSTRACT
Ethanol (EtOH) modulation of central amygdala (CeA) neurocircuitry plays a key role in the development of alcoholism via activation of the corticotropin-releasing factor (CRF) receptor (CRFR) system. Previous work has predominantly focused on EtOH × CRF interactions on the CeA GABA circuitry; however, our laboratory recently showed that CRF enhances CeA glutamatergic transmission. Therefore, this study sought to determine whether EtOH modulates CeA glutamate transmission via activation of CRF signaling.