GSE171683
Vitamin D deficiency exacerbates UV/endorphin and opioid addiction
Due to the current opioid epidemic, a better understanding of genetic and environmental factors that contribute to opioid addiction is warranted. To explore the potential causative role of VitD in opioid addiction , we used multiple pharmacologic approaches and genetic mouse models. We used profiled the transcriptome of key brain reward regions upon morphine treatment in vitamin D receptor KO and wild type mice. Our results highlight the role of VitD deficiency in the development of addiction and suggest a potential therapeutic benefit of VitD supplementation for VitD deficient individuals in the prevention and management of addiction. Overall design: To examine the mechanism underlying the increased morphine reward in Vdr-/- mice, we performed RNA-seq on bilateral micro-punches of the nucleus accumbens and the ventral tegmental area, key brain regions for morphine reward, from Vdr-/- and wild type mice i.p. injection of PBS or 5 mg/kg morphine sulfate. Mice were sacrificed with cervical dislocation. Brains were then immediately flash frozen in isopentane and stored in -80°C. Punches were taken from coronal sections of the mouse brain for both NACC and VTA. For NACC, the aci and fmi white matter structures were used as landmarks to determine Bregma 1.94. 1.5 mm diameter bilateral punches were then taken 2 mm in depth with aci at the center of the punch, to ensure both the accumbens core and shell were within the punch. To reach the VTA, coronal sections were taken until white matter structures of the cingulum (cg) were rounded and the dentate gyrus of the hippocampus began to form ventrally and caudally, as observed at Bregma -2.92 mm. 1.5 mm diameter bilateral punches were then taken at ~1.0 mm in depth at a location 0.5 mm lateral and from the the midsagittal plane and 0.5 mm from the most ventral portion of the brain.