Additionally, while BDNF is strongly regulated by serotonin levels and inherited serotonin transporter down-regulation is associated with increased vulnerability to cocaine addiction, the effects of serotonin transporter genotype on BDNF signaling in the amygdala under naïve and cocaine exposure conditions are unknown.
Thus, activity in the PrL-NAc pathway is responsible for the therapeutic effect of BDNF on cocaine-seeking whereas inhibition of activity in the PrL-pPVT pathway elicits a similar therapeutic effect in the absence of BDNF.<b>SIGNIFICANCE STATEMENT</b> The major issue in cocaine addiction is the high rate of relapse.
Cocaine-induced chromatin remodeling increases brain-derived neurotrophic factor transcription in the rat medial prefrontal cortex, which alters the reinforcing efficacy of cocaine.
Cocaine-induced chromatin remodeling increases brain-derived neurotrophic factor transcription in the rat medial prefrontal cortex, which alters the reinforcing efficacy of cocaine.
A single infusion of brain-derived neurotrophic factor into the ventral tegmental area induces long-lasting potentiation of cocaine seeking after withdrawal.
A single infusion of brain-derived neurotrophic factor into the ventral tegmental area induces long-lasting potentiation of cocaine seeking after withdrawal.