The endogenous role of BDNF/TrkB activity in the insular cortex during methylphenidate-induced taste avoidance

Drug intake is thought to reflect an affective balance, such that a drug's rewarding effects increase the propensity for use, while its aversive effects limit it. A common behavioral assay to assess the aversive effects of drugs is the conditioned taste avoidance procedure (CTA). The insular cortex (IC) is believed to be a critical center for higher order processing of CTA learning and the activity in this region of brain derived neurotrophic factor (BDNF) and its receptor, the tropomyosin related kinase receptor type B (TrkB), has been repeatedly demonstrated to be involved in the phenomenon. The present set of studies examined the endogenous role of IC BDNF/TrkB in CTA induced by methylphenidate (MPH) via employment of two behavioral manipulations known to alter a CTA's strength (i.e., age effects and preexposure effects), followed by assessment of the expression of BDNF, TrkB and its activated form, pTrkB, using Western blots. IC BDNF/TrkB was found to both potentiate and attenuate the strength of CTA learning, which appeared to depend upon its relative concentration and temporal relation to other CTA related signaling cascades in the region. Implications and future directions are discussed.