{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T11:00:17Z","timestamp":1774090817219,"version":"3.50.1"},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,3,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Hypothesis<\/jats:title>\n                    <jats:p>Allele-specific expression (ASE) of long non-coding RNAs (lncRNAs) links genetic variation to synaptic dysfunction in psychiatric disorders. We previously identified a disease-associated ASE shift in LINC02449 at rs149707223 (C\/G), with preferential expression of the alternative G allele in bipolar disorder (BD) and schizophrenia (SZ). Overexpression of LINC02449-G induced social deficits, repetitive behaviors, and enhanced excitatory synaptic transmission in the medial prefrontal cortex-nucleus accumbens (mPFC-NAc) circuit via upregulation of CPLX1. We hypothesized that these abnormalities are mediated by glutamatergic hyperexcitability and are pharmacologically reversible.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Study Design<\/jats:title>\n                    <jats:p>Adult C57BL\/6 mice received mPFC-targeted AAV-mediated LINC02449-G overexpression followed by systemic administration of Riluzole. Molecular, behavioral, and electrophysiological analyses were performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Study Results<\/jats:title>\n                    <jats:p>Riluzole dose-dependently normalized elevated Cplx1 expression induced by LINC02449-G in mice. Behavioral assays showed significant rescue of social interaction deficits and reductions in excessive grooming and marble-burying behavior. Whole-cell recordings revealed that Riluzole restored increased mEPSC frequency and amplitude in NAc neurons to control levels, indicating correction of mPFC-NAc circuit hyperexcitability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These results demonstrate that synaptic and behavioral abnormalities caused by ASE-driven lncRNA dysregulation are pharmacologically reversible. Riluzole represents a promising candidate for repurposing in neuropsychiatric disorders characterized by glutamatergic imbalance and frontostriatal circuit dysfunction, and highlights ASE-regulated lncRNAs as actionable therapeutic targets.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/schbul\/sbag021","type":"journal-article","created":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T10:20:15Z","timestamp":1774088415000},"source":"Crossref","is-referenced-by-count":0,"title":["Riluzole Restores Circuit and Behavioral Function Altered by Allele-Specific Expression-Mediated LINC02449\u2013CPLX1 Dysregulation"],"prefix":"10.1093","volume":"52","author":[{"given":"Chaoying","family":"Ni","sequence":"first","affiliation":[{"name":"Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong-Hong Kong Joint Laboratory for Psychiatric Disorders, Guangdong Province 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