A BDNF infusion into the medial prefrontal cortex suppresses cocaine-seeking in rats
Brain-derived neurotrophic factor (BDNF) is released from neurons to promote communication between neurons. The levels of BDNF are increased in various brain regions after chronic cocaine administration and this increase has been presumed to mediate the development of addictive behaviors, such as the excessive drive to obtain cocaine and the vulnerability to relapse in addicts. In contrast, a recent study by NARC scientists shows that BDNF can actually relieve this drug-seeking behavioral pathology. The key is to administer BDNF into the prefrontal cortex where BDNF can travel down the prefrontal axon connections to the nucleus accumbens and alter glutamate release. In this manner, BDNF inhibits relapse in an animal model, perhaps by remodeling the connections from the prefrontal cortex to the nucleus accumbens.
Figure 1. Intra-dmPFC BDNF attenuates cocaine-seeking in rats. Top: experimental design. Bottom: A) The number of lever presses 6 days after the BDNF infusion administered immediately after the last of 10 cocaine self-administration sessions is reduced. Bottom: B) The number of lever presses elicited by a tone/light conditioned cue after 6 days of extinction training is reduced. C) The number of lever presses elicited by cocaine prime-induced reinstatement of cocaine-seeking is reduced (adapted from Berglind et al., 2007).
Figure 2. Intra-prefrontal BDNF infusion prevents basal and cocaine prime-induced increase in dialysis glutamate levels in nucleus accumbens.
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