These observations demonstrate a crucial function for Erbin in AMPAR surface expression in cortical PV-positive interneurons and may contribute to a better understanding of psychiatric disorders.
Posttranscriptional regulation is therefore necessary to retain the transcriptional identity and support functional specialization of the proprioceptive sensory neurons.<b>NEW & NOTEWORTHY</b> We have demonstrated that selectively impairing Dicer in parvalbumin-positive neurons, which include the proprioceptors, triggers behavioral changes, a lack of muscle connectivity, and a loss of transcriptional identity as observed through RNA sequencing.
Our findings suggest that the susceptibility of parvalbumin neurons to stress may represent a key mechanism contributing to functional and structural impairments in specific brain regions relevant for psychiatric disorders.
Parvalbumin-positive (PV+) neurons in the cerebral cortex, mostly corresponding to fast-spiking basket cells, have been implicated in higher-order brain functions and psychiatric disorders.
Exposure to prenatal stress (PS) and mutations in <i>Gad1</i>, which encodes GABA synthesizing enzyme glutamate decarboxylase (GAD) 67, are the primary risk factors for psychiatric disorders associated with abnormalities in parvalbumin (PV)-positive GABAergic interneurons in the medial prefrontal cortex (mPFC).
Treatment with anti-inflammatory compounds, such as D-serine, 7,8-dihydroxyflavone (a TrkB agonist), sulforaphane (or its precursor glucoraphanin), and TPPU (1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea: a soluble epoxide hydrolase inhibitor), during adolescence might prevent the onset of behavioral abnormalities and parvalbumin immunoreactivity in the medial prefrontal cortex of adult offspring after MIA.