title: Molecular mechanisms of autism: a possible role for Ca2+ signaling.
abstract: Autism spectrum disorders (ASDs) are a group of developmental disorders characterized by social and emotional deficits, language impairments and stereotyped behaviors that manifest in early postnatal life. The molecular mechanisms that underlie ASDs are not known, but several recent developments suggest that some forms of autism are caused by failures in activity-dependent regulation of neural development. Mutations of several voltage-gated and ligand-gated ion channels that regulate neuronal excitability and Ca2+ signaling have been associated with ASDs. In addition, Ca2+-regulated signaling proteins involved in synapse formation and dendritic growth have been implicated in ASDs. These recent advances suggest a set of signaling pathways that might have a role in generating these increasingly prevalent disorders.
authors.affiliation: Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
authors.forename: Jocelyn F
authors.initials: JF
authors.lastname: Krey
authors.forename: Ricardo E
authors.initials: RE
authors.lastname: Dolmetsch
mesh_terms: D001321:Autistic Disorder / Q000209:etiology* / Q000503:physiopathology*; D001921:Brain / Q000254:growth & development* / Q000378:metabolism / Q000503:physiopathology*; D020013:Calcium Signaling / Q000235:genetics*; D002454:Cell Differentiation / Q000235:genetics; D004777:Environment; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D017981:Receptors, Neurotransmitter / Q000378:metabolism; D013569:Synapses / Q000378:metabolism; D009435:Synaptic Transmission / Q000235:genetics*
chemical_list: D007473:Ion Channels; D017981:Receptors, Neurotransmitter