期刊
NEUROPSYCHOPHARMACOLOGY
卷 43, 期 10, 页码 2075-2082出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41386-018-0049-1
关键词
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资金
- NIDA [R00 DA031699]
- NIH
- Alzheimer's Drug Discovery Foundation
- Harrington Discovery Institute
- Thome Alzheimer's Disease Drug Discovery Foundation
- Brain & Behavior Research Foundation
- Michael J. Fox Foundation
- Dystonia Medical Research Foundation
- CHDI Foundation
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(5) but not mGlu(1) and was specific for D1(+) MSNs, whereas PFC LTD was expressed at both D1(+) and D1(-) MSNs and required mGlu(1) but not mGlu(5). Two weeks after five daily non-contingent cocaine exposures (15 mg/kg), LTD was attenuated at MDT-D1(+) synapses but was rescued by the mGlu(5)-positive allosteric modulator (PAM) VU0409551. These results highlight unique plasticity mechanisms regulating specific NAcSh synapses.
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