Alcohol, clinical & experimental research · 2026
Ethanol effects on excitability of corticotropin-releasing factor-expressing neurons in the medial subdivision of the mouse central amygdala nucleus.
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Li Qiang, Klein Rebecca, Moore Scott D
Аннотация
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 (CeMCRF) in the CeM and measured intrinsic measures of excitability in response to acute ethanol exposure.
RESULTS: We found that CeMCRF 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 CeMCRF neurons during repetitive firing. Ethanol's inhibitory effect on neuronal excitability persists even in synaptically isolated CeMCRF 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 CeMCRF 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 CeMCRF neurons within stress-related amygdala circuits.
METHODS: We performed whole-cell patch clamp recordings on identified CRF-containing neurons (CeMCRF) in the CeM and measured intrinsic measures of excitability in response to acute ethanol exposure.
RESULTS: We found that CeMCRF 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 CeMCRF neurons during repetitive firing. Ethanol's inhibitory effect on neuronal excitability persists even in synaptically isolated CeMCRF 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 CeMCRF 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 CeMCRF neurons within stress-related amygdala circuits.