ArticleNeuropharmacology2026
Acute ethanol inhibits asynchronous glutamate release from mouse basolateral amygdala synapses.
Article in Neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute ethanol modulates an incredibly diverse number of neurotransmitter receptors and intracellular pathways. Presynaptic modulation by acute ethanol has been identified at some GABAergic synapses; but descriptions of acute ethanol regulation of presynaptic glutamatergic function are sparse. Recent reports suggest that acute ethanol can inhibit glutamatergic synaptic responses arising from recycling vesicles during tetanic stimulation of Stria terminalis inputs onto basolateral amygdala (BLA) principal neurons. This finding gives rise to the hypothesis that acute ethanol may modulate actively priming synaptic vesicles in glutamate synapses. To test this, we used whole cell patch clamp recordings in BLA principal neurons and measured the effects of acute ethanol on asynchronous synaptic transmission. We found Stria teminalis inputs express EGTA-sensitive asynchronous synaptic glutamatergic responses produced from both increased presynaptic activation and experimental elevation of presynaptic calcium using partial substitution of extracellular Na
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