Alcoholism is a chronic disorder characterized by the appearance of a withdrawal syndrome consequent to the abrupt cessation of prolonged alcohol consumption. Among all the symptoms, anxiety seems to be the most prevalent. For individuals who have some anxiety disorder, ethyl alcohol is a strong reinforcer and its effects on the inhibitory control of behavior can be modulated by context. In addition, as in humans, rats segregated in function of their anxiety levels (genotypic or phenotypic) differ significantly. Among the neural processes underlying these changes are the serotonergic (5-HT) and dopaminergic (DA) neurotransmission. Among the structures involved in behavioral and affective dysregulation induced by alcohol intake and withdrawal several studies point out the role of the mechanisms of the medial prefrontal cortex (mPFC) on the modulation of subcortical areas known to be involved in the motivational and emotional aspects of alcohol use and abuse, as the nucleus accumbens and amygdala. Moreover, alcohol-induced changes appear to be greatly modulated by the emotional state of the individual, and, as noted elsewhere, by the contextual clues present during drug reinforcement. In this project we will evaluate the role of the (PrL) and infralimbic (IL) subdivisions of the PFC on the expression of the aversive effects of withdrawal of alcohol, using the experimental paradigm of fear-potentiated startle. Changes in these brain regions are commonly linked to the modulation of physiological responses of fear evoked in subcortical areas, including the amygdala.
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