Effect of medial prefrontal cortex 6-OHDA lesions on behavioral and neurochemical responses to gustatory stimuli

Appetitive sweet tastes increase dopamine (DA) in the nucleus accumbens (NAc) shell and core and in the medial prefrontal cortex (mPFC) in relation to their motivational valence, salience and novelty; the DA increase in the NAc shell is subjected to single trial habituation while in the NAc core and in the mPFC is not. Recently it was shown that sensitization to morphine can reverse these phenomena in the NAc shell and in the mPFC; abolishment of the habituation phenomenon was observed in the NAc shell while in the mPFC single trial habituation took place. Medial prefrontal cortex is an area well known to interact with subcortical areas such as the VTA and the NAc and it has been proposed that DA depletion in the mPFC can alter the mode of function of subcortical areas, including the NAc DAergic responses to pharmacological and environmental challenges of the system. In fact, 6-OHDA lesions of the mPFC have been shown to produce sensitization to the neurochemical and behavioral responses to cocaine and to alter the NAc DAergic transmission in response to natural reinforcers. In the present thesis it was studied the effect of 6-OHDA lesions in the mPFC in the NAc DAergic response to a taste stimulus (sweet chocolate) using in vivo microdialysis. Moreover, behavioral taste reactivity and motor behavior studies were held out to investigate whether the lesions influence this type of behaviors. As in sensitized to morphine animals, lesions produced abolishment of habituation in the NAc shell in the pre-exposed to taste animals, while in the NAc core produced a higher and delayed increase in DA in the naive animals. No differences between lesioned and sham operated animals where observed in naive and pre-exposed animals in the DAergic response of NAc shell and core, respectively. No differences were observed between the groups in taste reactivity test and in the motor activity studies. TH immunoreactivity studies were performed and tissue neurotransmitter levels were quantified in order to evaluate the extension and percentage of the lesions in the mPFC.