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mGlu and mGlu modulate distinct excitatory inputs to the nucleus accumbens shell.

Turner BD, Rook JM, Lindsley CW, Conn PJ, Grueter BA
Neuropsychopharmacology. 2018 43 (10): 2075-2082

PMID: 29654259 · PMCID: PMC6097986 · DOI:10.1038/s41386-018-0049-1

Glutamatergic transmission in the nucleus accumbens shell (NAcSh) is a substrate for reward learning and motivation. Metabotropic glutamate (mGlu) receptors regulate NAcSh synaptic strength by inducing long-term depression (LTD). Inputs from prefrontal cortex (PFC) and medio-dorsal thalamus (MDT) drive opposing motivated behaviors yet mGlu receptor regulation of these synapses is unexplored. We examined Group I mGlu receptor regulation of PFC and MDT glutamatergic synapses onto specific populations of NAc medium spiny neurons (MSNs) using D1tdTom BAC transgenic mice and optogenetics. Synaptically evoked long-term depression (LTD) at MDT-NAcSh synapses required mGlu but not mGlu and was specific for D1(+) MSNs, whereas PFC LTD was expressed at both D1(+) and D1(-) MSNs and required mGlu but not mGlu. Two weeks after five daily non-contingent cocaine exposures (15 mg/kg), LTD was attenuated at MDT-D1(+) synapses but was rescued by the mGlu5-positive allosteric modulator (PAM) VU0409551. These results highlight unique plasticity mechanisms regulating specific NAcSh synapses.

MeSH Terms (19)

Animals Cocaine Female Mediodorsal Thalamic Nucleus Mice Mice, Inbred C57BL Mice, Transgenic Motor Activity Neuronal Plasticity Neurons Nucleus Accumbens Optogenetics Oxazoles Prefrontal Cortex Pyridines Receptor, Metabotropic Glutamate 5 Receptors, Metabotropic Glutamate Synapses Synaptic Transmission

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