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Neuropharmacology. 2019 Jan;144:1-8. doi: 10.1016/j.neuropharm.2018.10.010. Epub 2018 Oct 12.

An Aplysia-like synaptic switch for rapid protection against ethanol-induced synaptic inhibition in a mammalian habit circuit.

Author information

1
Department of Pharmacology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
2
Department of Pharmacology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA. Electronic address: bmathur@som.umaryland.edu.

Abstract

Decades of work in Aplysia californica established the general rule that principles of synaptic plasticity and their molecular mechanisms are evolutionarily conserved from mollusks to mammals. However, an exquisitely sensitive, activity-dependent homosynaptic mechanism that protects against the depression of neurotransmitter release in Aplysia sensory neuron terminals has, to date, not been uncovered in other animals, including mammals. Here, we discover that depression at a mammalian synapse that is implicated in habit formation and habit learning acceleration by ethanol, the fast-spiking interneuron (FSI) to medium spiny principal projection neuron (MSN) synapse of the dorsolateral striatum, is subject to this type of synaptic protection. We show that this protection against synaptic depression is calcium- and PDZ domain interaction-dependent. These findings support activity dependent protection against synaptic depression as an Aplysia-like synaptic switch in mammals that may represent a leveraging point for treating alcohol use disorders.

KEYWORDS:

Alcohol; Delta opioid receptor; FSI; LTD; MSN; PKA; PKC; Parvalbumin; Striatum

PMID:
30321611
PMCID:
PMC6286215
DOI:
10.1016/j.neuropharm.2018.10.010
[Indexed for MEDLINE]
Free PMC Article

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