Abstract

The bed nucleus of the stria terminalis (BNST) is a subcortical structure ideally organized to filter and/or integrate multiple modalities and translate the adequate resolution to motor systems for adaptive physiological and behavioral outcomes. Evidence shows that alterations in synaptic transmission in certain regions of the BNST contribute significantly in cocaine intake behaviors, at least in rodent models. Specifically, exaggerated enhancement in transmission at BNST excitatory synapses has been clearly linked to cocaine self-administration in rats. Neurochemicals such as norepinephrine and corticotropin-releasing factor potentiate even further excitatory synaptic transmission in the BNST to trigger relapse to cocaine seeking induced by stressors like electrical footshock. Finally, dysregulation at BNST inhibitory synapses also occurs in rats with history of cocaine self-administration and may encode individual motivation to seek and take cocaine. It is clear the BNST plays an important role in the manifestation of cocaine intake behavior and thus our understanding of its maladaptive plasticity changes are an important puzzle piece to the system that generates addictive disorders.

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