Development of sensitization to methamphetamine in offspring prenatally exposed to morphine, methadone and buprenorphine. (3rd April 2013)

• Record Type: Journal Article
• Authors: Chiang, Yao‐Chang; Hung, Tsai‐Wei; Ho, Ing‐Kang
• Is Part Of: Addiction biology. Volume 19:Number 4(2014:Jul.)
• Page Start: 676
• Page End: 686
• Publication Date: 2013-04-03
• Subjects: Substance abuse -- Periodicals; Substance abuse -- Physiological aspects -- Periodicals; Substance-Related Disorders -- periodicals; 616.86
• DOI: 10.1111/adb.12055
• Languages: English
• ISSNs: 1355-6215

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>Heroin use among young women of reproductive age has drawn much attention around the world. However, there is lack of information on the long‐term effects of prenatal exposure to opioids on their offspring. Our previous study demonstrated that prenatally buprenorphine‐exposed offspring showed a marked change in the cross‐tolerance to morphine compared with other groups. In the current study, this animal model was used to study effects of methamphetamine (METH)‐induced behavioral sensitization in the offspring at their adulthood. The results showed no differences in either basal or acute METH‐induced locomotor activity in any of the groups of animals tested. When male offspring received METH injections of 2 mg/kg, i.p., once a day for 5 days, behavioral sensitization was induced, as determined by motor activity. Furthermore, the distance and rate of development (slope) of locomotor activity and conditioned place preference induced by METH were significantly increased in the prenatally buprenorphine‐exposed animals compared with those in other groups. The dopamine D<sub>1</sub>R in the nucleus accumbens of the prenatally buprenorphine‐exposed offspring had lower mRNA expression; but no significant changes in the μ‐, κ‐opioid, nociceptin, D<sub>2</sub>R and D<sub>3</sub>R receptors were noted. Furthermore, significant alterations were observed in the basal level of cAMP and the D<sub>1</sub>R agonist enhanced adenylyl cyclase activity in the prenatally buprenorphine‐exposed group. Overall, the study demonstrates that D<sub>1</sub>R and its downregulated cAMP signals are involved in enhancing METH‐induced behavioral sensitization in prenatally buprenorphine‐exposed offspring. The study reveals that prenatal exposure to buprenorphine caused long‐term effects on offspring and affected the dopaminergic system‐related reward mechanism.</p> </abstract>