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Updated: Jul 15, 2026
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Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication
Published on: February 6, 2019
Ethanol inhibits persistent activity in prefrontal cortical neurons
Yali Tu1, Sven Kroener, Kenneth Abernathy
1Department of Neurosciences and Center for Drug and Alcohol Programs, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Summary
Ethanol disrupts prefrontal cortex (PFC) neuron activity, reducing spike firing and persistent network patterns. These effects may be linked to dopamine D1 receptor activity and contribute to alcohol-related behavioral changes.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Alcohol consumption impairs cognitive functions regulated by the prefrontal cortex (PFC).
- Mechanisms underlying alcohol's effects on PFC neuronal activity remain largely unknown.
Purpose of the Study:
- To investigate the impact of ethanol on neuronal firing and network activity in the PFC.
- To elucidate the electrophysiological mechanisms of ethanol's effects on PFC neurons.
Main Methods:
- In vivo and in vitro electrophysiology in anesthetized rats and PFC coculture systems.
- Multielectrode extracellular recordings and analysis of persistent neuronal activity.
- Application of ethanol, NMDA antagonist APV, and D1 dopamine receptor antagonist SCH23390.
Main Results:
- Ethanol dose-dependently reduced PFC neuronal spike activity in vivo.
- In vitro, ethanol inhibited persistent PFC neuronal activity, with enhanced activity post-washout.
- NMDA antagonist APV mimicked ethanol's inhibitory effect; D1 receptor antagonism potentiated ethanol's inhibition.
Conclusions:
- Ethanol inhibits persistent activity and spike firing in PFC neurons.
- Ethanol's effects on PFC neurons may be modulated by D1 dopamine receptor tone.
- Altered deep-layer cortical neuron activity by ethanol could explain behavioral effects of alcohol intake.
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