Both mentalization and empathy allow humans to understand others, through the representation of their mental states or their mood, respectively. The present review aims to explain those characteristics which are shared between empathy and the Theory of Mind. Research in neuroscience, based on naturalistic paradigms, has shown that abilities to mentalize and to empathize are associated with the activation of different neuro-cognitive circuits. As far as mirror-neuron processes are concerned, some structures (like Anterior Insula, AI; Anterior Cingulate Cortex, ACC) play a role both in the representation of one’s own affective states and in comprehension of the same affective state when experienced by others. As for mentalization, the temporal parietal junction (TPj) and temporal poles (TP), the upper posterior temporal sulcus (pSTS) and the medial prefrontal cortex (mPFC) are greatly involved: the latter appears involved in the attribution of one’s own and others’ temperaments. Interestingly, the ventral/orbital portion of the PFC (orbito-frontal cortex, OFC) is involved in subserving shared affective experience during cognitive mentalizing. This brain region represents a point of overlap, from a psycho-biological point of view, where emotional mirroring and affective cognition meet up. As for animal models, laboratory rodents can well be tested for prosocial behavior. Some examples include deliberate actions, allowing another conspecific the possibility to feed (“giving food”): this willingness can vary across donors, depending on how the recipient is perceived. Other examples include the possibility to let a trapped conspecific come out (“giving help”). The state-of-the-art knowledge about this theme can inform the programming of specific clinical interventions, based on the reinforcement of empathic and/or mentalization abilities.
Compulsivity is defined as an unstoppable tendency toward repetitive and habitual actions, which are reiterated despite negative consequences. Polydipsia is induced preclinically by intermittent reward, leading rodents to ingest large amounts of fluids. We focused on the role of dopamine transporter (DAT) and inheritance factors in compulsive behavior. Our sample consisted of DAT heterozygous (HET) rats with different genetic inheritance (MAT‐HET, born from WT‐dams × KO‐fathers; MIX‐HET, born from HET‐dams × KO‐fathers). As controls, we used both wild‐type (WT) rats and their socially‐isolated (WTi) siblings. We ran the schedule‐induced polydipsia (SIP) protocol, to induce compulsive behavior; then the Y‐maze and marble‐burying tests, to verify its actual development. Only MAT‐HET (who inherited the functional DAT allele from the WT mother) is vulnerable to developing compulsive behavior. MAT‐HET rats drank increasingly more water during SIP; they showed significant perseverance in the Y‐maze test and exhibited compulsive actions in the marble‐burying test. Interestingly, compulsive behaviors of MAT‐HET rats correlated with expression ex vivo of different genes in different areas. Regarding the prefrontal cortex (PFC), D2R correlated with Y‐maze “perseverance” in addition to BDNF; considering the amygdala (AMY), both D3R and OXTR correlated with SIP “licks.” Indeed, compulsivity may be linked to D2R and BDNF in PFC, while extreme anxiety in MAT‐HET rats may be associated with D3R and OXTR in the AMY. These results confirm some similarities between MAT‐HET and DAT‐KO subjects, and link the epigenetic context of the DAT gene to the development of compulsive behavior.
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