DOI: 10.1101/471011Nov 15, 2018Paper

Ethanol Experience Enhances Glutamatergic Ventral Hippocampal Inputs To D1 Receptor-Expressing Medium Spiny Neurons In The Nucleus Accumbens Shell

BioRxiv : the Preprint Server for Biology
Daniel M KircherRichard A Morrisett


Nucleus accumbens dopamine D1 receptor-expressing medium spiny neurons (D1-MSNs) have been implicated in the formation of dependence to many drugs of abuse including alcohol. Previous studies have revealed that acute alcohol exposure suppresses glutamatergic signaling within the accumbens and repeated alcohol exposure enhances glutamatergic signaling. D1-MSNs receive glutamatergic input from several brain regions and it is not currently known how individual inputs onto D1-MSNs are altered by alcohol experience. To Address this, we used virally mediated expression of Channelrhodopsin (ChR2) in ventral hippocampal (vHipp) glutamate neurons to selectively activate vHipp to D1-MSN synapses and compared synaptic adaptations in response to low and high alcohol experience in vitro and in vivo. Alcohol experience enhanced glutamatergic activity and abolished long-term depression (LTD) at ventral hippocampal (vHipp) to D1-MSN synapses. Following chronic alcohol experience GluA2-lacking AMPA receptors, which are Ca-permeable, were inserted into vHipp to D1-MSN synapses. These alcohol-induced adaptations of glutamatergic signaling occurred at lower levels of exposure than previously reported. The loss of LTD expression and enhancement in ...Continue Reading

Related Concepts

Alcoholic Intoxication, Chronic
Mental Depression
Drug Abuse
Hippocampus (Brain)
Nucleus Accumbens
Dopamine Receptor

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