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Transcriptomic Dysregulation in Rodent Models of ADHD and Substance Use Suggests Shared Neural Mechanisms
Van Horn, Sarah Driscoll, Heather Toufexis, Donna
Van Horn, Sarah
Driscoll, Heather
Toufexis, Donna
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Abstract
Attention-Deficit/Hyperactivity Disorder (ADHD) is highly heritable and increases the likelihood of substance abuse. The self-medication hypothesis of nicotine use in ADHD proposes that ADHD patients seek nicotine for its ability to improve their symptoms, and they have less success quitting, possibly due to the worsening of symptoms in withdrawal (Liebrenz et. al., 2014). By comparing the transcriptome of rodent models of ADHD to those of nicotine dependence (ND), the present analysis identified novel differentially expressed genes that may contribute to their high co-occurrence (PRKAG2, MAPK1), and genes with known associations to ADHD or ND (ANK3, CALD1, CHRNA4, CHRNA7, CMTM8, DLG4, DUSP6, GNG3, GNG11, GRIK5, GRINA2, ICAM2, KCNJ6, PRKAB1, SYNPO, VAMP2). MAPK signaling pathways (R HSA-5673001, R-HSA-5684996) and synaptic transmission (R-HAS-112315) were enriched in both ADHD and ND. These pathways mediate neurological mechanisms that contribute to ND.
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2024-01-01