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. 2015 Aug 12;41(4):949–959. doi: 10.1038/npp.2015.221

Figure 2.

Figure 2

Chronic opioid treatment stimulates BDNF expression in the VTA that contributes to a blunted cocaine place preference. (a) BDNF mRNA (green) was detected with fluorescent in situ hybridization in both microglial (blue, identified with itgam promoter; white arrow) and non-microglial cells (yellow arrow). Chronic morphine caused an increase in BDNF transcripts in the VTA sections from opioid-dependent animals. (b) Total BDNF mRNA in VTA sections was semi-quantified using image analysis (see methods), and BDNF levels were significantly elevated in the VTA of opioid-dependent animals. Error bars=SEM, *p<0.05, n=4. (c) Tissue punches from the VTA were analyzed for BDNF protein expression using western blot analysis. Opioid-dependent animals showed an increase in BDNF protein (normalized to beta-actin) that was significantly greater than opioid-naïve brains. Minocycline reduced BDNF expression in the VTA of opioid-dependent animals. Error bars=SEM, *p<0.05, n=5. (d) Bilateral infusion of BDNF into the VTA of opioid-naïve animals prior to cocaine conditioning blocked the expression of cocaine place preference. Systemic injection with a potent trkB agonist, 7,8-dihydroxyflavone, enhanced cocaine CPP in opioid-naïve animals, compared with animals treated with vehicle. Error bars=SEM, *p<0.05 when compared with vehicle, ##p<0.01, when compared with baseline, n=6–8.