2026/01/01 by Qiang Li, Rebecca Klein, Scott D. Moore · 1 voice
Neuroscience · #Memory and Neural Mechanisms #Neuroscience and Neuropharmacology Research #Neurotransmitter Receptor Influence on Behavior
paper · pdf · doi:10.1111/acer.70234
openalex publication_date 2026/01/01 · openalex created_date 2026/01/20 · openalex updated_date 2026/07/28
Abstract Background Corticotropin‐releasing factor (CRF) neurons in the medial subdivision of the central amygdala (CeM) are a distinct subpopulation of neurons in a critical brain region modulating ethanol actions. Previous studies have demonstrated enhanced release of GABA and neuropeptides in this brain region in response to acute ethanol exposure. Methods We performed whole‐cell patch clamp recordings on identified CRF‐containing neurons (CeM CRF ) in the CeM and measured intrinsic measures of excitability in response to acute ethanol exposure. Results We found that CeM CRF neurons are highly sensitive to actions of acute ethanol exposure, which suppresses neuronal excitability in a dose‐dependent manner and shortens spike duration of the CeM CRF neurons during repetitive firing. Ethanol's inhibitory effect on neuronal excitability persists even in synaptically isolated CeM CRF neurons, an indication of a direct action on the intrinsic membrane properties that underlie excitability. Conclusions Our results reveal that ethanol selectively alters intrinsic firing mechanisms of CeM CRF neurons at low dose but broadly suppresses excitability at a higher dose. These findings provide new insight into how alcohol modulates intrinsic membrane properties of these CeM CRF neurons within stress‐related amygdala circuits.