"Empathy plays a fundamental social role, allowing the sharing of experiences, needs, and goals across individuals. Anxiety, posttraumatic stress disorder, autism, Asperger's syndrome and some cerebral damage are often characterised by an inability to empathise with others. Some studies of animal behaviour claim that empathy is not restricted to humans, and even rodents have been shown to demonstrate empathy for cagemates in pain. It is very likely that pro-social behaviour has neurological and neurochemical basis. Although recent fMRI studies on humans revealed that experience of empathy connected with activity of several regions in cerebral cortex, the molecular mechanism of empathy is still poorly understood. The current project is aimed to study the signal transduction pathways in brain involved in empathy. Given the intrinsic difficulties associated with such studies in human beings, here it is proposed to use an animal model, namely mice acutely treated with low dose of empathogens-entactogens, pharmacological agents that able to increase empathy, emotional sensitivity, loss of social inhibitions, reduced anxiety and an increased sense of closeness with other. Alteration in gene/protein expression profile of mouse cerebral cortex after single administration of widely used empathogen 1-(1,3-benzodioxol-5-yl)-N-methylpropan-2-amine will be investigated by methods of differential transcriptomics and proteomics. The co-administration of selective antagonists for 5-HT1a and oxytocin receptors, have been reported to regulate pro-social behaviour, will allow to distinguish between empathogenic and adverse effect of 1-(1,3-benzodioxol-5-yl)-N-methylpropan-2-amine. This study will further improve our knowledge about molecular mechanisms of empathy, and, possibly, may assist in elimination of side effects of existing empathogens-entactogens and in developing of therapies for patients suffering from specific neuronal pathologies."
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