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- W2777325040 abstract "Stress can precipitate or worsen symptoms of many psychiatric disorders by dysregulating glutamatergic function within the prefrontal cortex (PFC). Previous studies suggest that antagonists of group II metabotropic glutamate (mGlu) receptors (mGlu2 and mGlu3) reduce stress-induced anhedonia through actions in the PFC, but the mechanisms by which these receptors act are not known. We now report that activation of mGlu3 induces long-term depression (LTD) of excitatory transmission in the PFC at inputs from the basolateral amygdala. Our data suggest mGlu3-LTD is mediated by postsynaptic AMPAR internalization in PFC pyramidal cells, and we observed a profound impairment in mGlu3-LTD following a single, 20-min restraint stress exposure. Finally, blocking mGlu3 activation in vivo prevented the stress-induced maladaptive changes to amydalo-cortical physiology and motivated behavior. These data demonstrate that mGlu3 mediates stress-induced physiological and behavioral impairments and further support the potential for mGlu3 modulation as a treatment for stress-related psychiatric disorders." @default.
- W2777325040 created "2018-01-05" @default.
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- W2777325040 creator A5077644333 @default.
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- W2777325040 date "2017-12-21" @default.
- W2777325040 modified "2023-10-14" @default.
- W2777325040 title "Metabotropic glutamate receptor subtype 3 gates acute stress-induced dysregulation of amygdalo-cortical function" @default.
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- W2777325040 doi "https://doi.org/10.1038/s41380-017-0015-z" @default.
- W2777325040 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6013320" @default.
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- W2777325040 hasPublicationYear "2017" @default.
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