Abstract
An accumulating body of evidence indicates a tight relationship between the endocrine system and abnormal social behavior. Two evolutionarily conserved hypothalamic peptides, oxytocin and arginine-vasopressin, because of their extensively documented function in supporting and regulating affiliative and socio-emotional responses, have attracted great interest for their critical implications for autism spectrum disorders (ASD). A large number of controlled trials demonstrated that exogenous oxytocin or arginine-vasopressin administration can mitigate social behavior impairment in ASD. Furthermore, there exists long-standing evidence of severe socioemotional dysfunctions after hypothalamic lesions in animals and humans. However, despite the major role of the hypothalamus for the synthesis and release of oxytocin and vasopressin, and the evident hypothalamic implication in affiliative behavior in animals and humans, a rather small number of neuroimaging studies showed an association between this region and socioemotional responses in ASD. This review aims to provide a critical synthesis of evidences linking alterations of the hypothalamus with impaired social cognition and behavior in ASD by integrating results of both anatomical and functional studies in individuals with ASD as well as in healthy carriers of oxytocin receptor (OXTR) genetic risk variant for ASD. Current findings, although limited, indicate that morphofunctional anomalies are implicated in the pathophysiology of ASD and call for further investigations aiming to elucidate anatomical and functional properties of hypothalamic nuclei underlying atypical socioemotional behavior in ASD.
Highlights
Autism spectrum disorders (ASD) are neurodevelopmental disorders with complex and diversified pathogenesis characterized by dramatic impairment of social communication, social interaction and empathy with an estimated prevalence in the general population ranging from 1 in 100 to 1 in 54 children [1]
Building on the above mentioned evidences, this review aims at providing a synthesis of neuroimaging investigations reporting morphofunctional alterations of the hypothalamus in ASD
The decreased modulation of hypothalamic nuclei activity along with negative functional connectivity between hypothalamus and left temporoparietal junction (lTPJ), a region associated with anthropomorphization—which is the tendency to attribute human traits to artificial agents—was observed when ASD individuals interacted with a human player, and when
Summary
Autism spectrum disorders (ASD) are neurodevelopmental disorders with complex and diversified pathogenesis characterized by dramatic impairment of social communication, social interaction and empathy with an estimated prevalence in the general population ranging from 1 in 100 to 1 in 54 children [1]. OT and AVP are synthesized by magnocellular neurons of the supraoptic and paraventricular nuclei of the hypothalamus that secret them into the peripheral blood circulation through the posterior pituitary gland These peptides act as neurotransmitters through the dendritic terminals of magnocellular neurons that release them into the hypothalamic extracellular fluid [39], and through parvocellular neurons projections to brainstem and subcortical regions, such as the amygdala, nucleus accumbens and hippocampus [40,41]. Despite the unquestionable key role of the hypothalamus in the production of the OT and AVP (Swanson and Sawchenko, 1983), the severe socioemotional dysfunctions caused by hypothalamic lesions, and the apparent association between hypothalamic neuropeptides and socio-affective responses in ASD and neurotypical population (NT), hypothalamic involvement remains elusive in most of neuroimaging investigations exploring the neural correlates of normal and abnormal human socioemotional behavior [56,57,58,59,60,61,62]. Some fundamental open questions aiming at elucidating the morphological and functional hypothalamic anomalies and their impact on social cognition and behavior in ASD will be proposed
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