{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Garbarino VR"],"funding":["NICHD NIH HHS","NIA NIH HHS","NIDA NIH HHS","NIMH NIH HHS"],"pagination":["85-99"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6345621"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["140"],"pubmed_abstract":["A variety of human and animal studies support the hypothesis that serotonin (5-hydroxytryptamine or 5-HT) system dysfunction is a contributing factor to the development of autism in some patients. However, many questions remain about how developmental manipulation of various components that influence 5-HT signaling (5-HT synthesis, transport, metabolism) persistently impair social behaviors. This review will summarize key aspects of central 5-HT function important for normal brain development, and review evidence implicating perinatal disruptions in 5-HT signaling in the pathophysiology of autism spectrum disorder. We discuss the importance, and relative dearth, of studies that explore the possible correlation to autism in the interactions between important intrinsic and extrinsic factors that may disrupt 5-HT homeostasis during development. In particular, we focus on exposure to 5-HT transport altering mechanisms such as selective serotonin-reuptake inhibitors or genetic polymorphisms in primary or auxiliary transporters of 5-HT, and how they relate to neurological stores of serotonin and its precursors. A deeper understanding of the many mechanisms by which 5-HT signaling can be disrupted, alone and in concert, may contribute to an improved understanding of the etiologies and heterogeneous nature of this disorder. We postulate that extreme bidirectional perturbations of these factors during development likely compound or synergize to facilitate enduring neurochemical changes resulting in insufficient or excessive 5-HT signaling, that could underlie the persistent behavioral characteristics of autism spectrum disorder."],"journal":["Pharmacological research"],"pubmed_title":["Extreme enhancement or depletion of serotonin transporter function and serotonin availability in autism spectrum disorder."],"pmcid":["PMC6345621"],"funding_grant_id":["R01 MH106978","R21 HD081261","T32 DA031115","T32 AG021890","R01 MH093320"],"pubmed_authors":["Daws LC","Garbarino VR","Gould GG","Gilman TL"],"additional_accession":[]},"is_claimable":false,"name":"Extreme enhancement or depletion of serotonin transporter function and serotonin availability in autism spectrum disorder.","description":"A variety of human and animal studies support the hypothesis that serotonin (5-hydroxytryptamine or 5-HT) system dysfunction is a contributing factor to the development of autism in some patients. However, many questions remain about how developmental manipulation of various components that influence 5-HT signaling (5-HT synthesis, transport, metabolism) persistently impair social behaviors. This review will summarize key aspects of central 5-HT function important for normal brain development, and review evidence implicating perinatal disruptions in 5-HT signaling in the pathophysiology of autism spectrum disorder. We discuss the importance, and relative dearth, of studies that explore the possible correlation to autism in the interactions between important intrinsic and extrinsic factors that may disrupt 5-HT homeostasis during development. In particular, we focus on exposure to 5-HT transport altering mechanisms such as selective serotonin-reuptake inhibitors or genetic polymorphisms in primary or auxiliary transporters of 5-HT, and how they relate to neurological stores of serotonin and its precursors. A deeper understanding of the many mechanisms by which 5-HT signaling can be disrupted, alone and in concert, may contribute to an improved understanding of the etiologies and heterogeneous nature of this disorder. We postulate that extreme bidirectional perturbations of these factors during development likely compound or synergize to facilitate enduring neurochemical changes resulting in insufficient or excessive 5-HT signaling, that could underlie the persistent behavioral characteristics of autism spectrum disorder.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2020-11-07T09:48:58Z","creation":"2020-11-07T09:48:58Z"},"accession":"S-EPMC6345621","cross_references":{"pubmed":["30009933"],"doi":["10.1016/j.phrs.2018.07.010"]}}