TY - JOUR
T1 - Molecular mechanisms of autism
T2 - a possible role for Ca2+ signaling
AU - Krey, Jocelyn F.
AU - Dolmetsch, Ricardo E.
N1 - Funding Information:
JFK is supported by a National Research Service Award (NRSA) predoctoral fellowship. RED is supported by National Institutes of Health (NIH) RO1 NS048564, by the McKnight Endowment for Neurosciences and by the Searle Scholars Fund.
PY - 2007/2
Y1 - 2007/2
N2 - 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.
AB - 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.
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U2 - 10.1016/j.conb.2007.01.010
DO - 10.1016/j.conb.2007.01.010
M3 - Review article
C2 - 17275285
AN - SCOPUS:33846878716
SN - 0959-4388
VL - 17
SP - 112
EP - 119
JO - Current Opinion in Neurobiology
JF - Current Opinion in Neurobiology
IS - 1
ER -