Research ReportCorticostriatal BDNF and alcohol addiction

- Corticostriatal BDNF keeps alcohol drinking in check.
- DLS BDNF reduces alcohol intake through MAPK induction of downstream effectors.
- Excessive alcohol consumption blunts corticostriatal BDNF.
- Cortical BDNF expression is blunted with high alcohol consumption via miRNAs.

Growth factors, long studied for their involvement in neuronal development and plasticity, also regulate responses to drugs of abuse, including alcohol. This review details the intricate interaction between the Brain-Derived Neurotrophic Factor (BDNF) and alcohol, and provides evidence to suggest that corticostriatal BDNF signaling acts to keep alcohol drinking in moderation. Specifically, we describe studies in rodent models suggesting that moderate consumption of alcohol increases BDNF levels in the dorsal striatum, which in turn act to suppress alcohol intake by activating a Mitogen-Activated Protein Kinase (MAPK)-dependent genomic mechanism. We further provide data to suggest that alcohol intake levels escalate when the endogenous corticostriatal BDNF pathway becomes dysregulated. Finally, we summarize recent studies suggesting that specific microRNAs targeting BDNF mRNA in the medial prefrontal cortex (mPFC) regulate the breakdown of the protective corticostriatal BDNF pathway.This article is part of a Special Issue entitled SI:Addiction circuits.