This is a competing renewal application for continuing support of our research program in Molecular Neurobiology and Developmental Disorders. The program consists of an administrative and scientific core serving five major investigative areas. Each area has as its central theme the application of molecular neurobiology to an understanding of developmental processes and their regulation. Studies in the Regulation of Serotonin and beta-adrenergic Receptors section examine the regulation of serotonin and beta-adrenergic receptor mRNA and G-protein coupling during development, as well as the regulation of these receptor mRNAs by antidepressants and drugs which alter neurotransmission. The work seeks to understand those factors which initiate and maintain receptor gene expression. The section on Enzyme Regulation focuses on hormonal and neuronal regulation of phenylethanolamine N-methyltransferase (PNMT) gene expression during development. These studies examine differences in prenatal and postnatal mechanisms regulating enzyme expression. The section on Developmental Neurobiology of Canine Narcolepsy uses an animal model of narcolepsy, an autosomal recessive disorder which afflicts young adolescents and children, to examine defects in cholinergic and alpha(1)-adrenergic receptors. The research strategy utilizes the differential maturation of the relevant neurotransmitter systems to help localize the specific neurochemical lesion(s). In the section on Characterization of Developmentally Regulated Genes, we are devising methods of isolating and characterizing genes which are expressed during discrete developmental epochs. We hope to identify those genes which regulate the architectural development of the cerebral cortex. Finally, the section on Molecular and Linkage Genetics of Infantile Autism describes work seeking to find a gene marker for infantile autism in multiple-incidence families.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Program Projects (P01)
Project #
2P01MH039437-06
Application #
3099040
Study Section
Special Emphasis Panel (SRCM (26))
Project Start
1985-03-01
Project End
1993-02-28
Budget Start
1990-04-01
Budget End
1991-02-28
Support Year
6
Fiscal Year
1990
Total Cost
Indirect Cost
Name
Stanford University
Department
Type
Schools of Medicine
DUNS #
800771545
City
Stanford
State
CA
Country
United States
Zip Code
94305
Tsang, Kathryn M; Croen, Lisa A; Torres, Anthony R et al. (2013) A genome-wide survey of transgenerational genetic effects in autism. PLoS One 8:e76978
Sampath, Srirangan; Bhat, Shambu; Gupta, Simone et al. (2013) Defining the contribution of CNTNAP2 to autism susceptibility. PLoS One 8:e77906
Fradin, Delphine; Cheslack-Postava, Keely; Ladd-Acosta, Christine et al. (2010) Parent-of-origin effects in autism identified through genome-wide linkage analysis of 16,000 SNPs. PLoS One 5:
Weiss, Lauren A; Arking, Dan E; Gene Discovery Project of Johns Hopkins & the Autism Consortium et al. (2009) A genome-wide linkage and association scan reveals novel loci for autism. Nature 461:802-8
Arking, Dan E; Cutler, David J; Brune, Camille W et al. (2008) A common genetic variant in the neurexin superfamily member CNTNAP2 increases familial risk of autism. Am J Hum Genet 82:160-4
Benayed, Rym; Gharani, Neda; Rossman, Ian et al. (2005) Support for the homeobox transcription factor gene ENGRAILED 2 as an autism spectrum disorder susceptibility locus. Am J Hum Genet 77:851-68
Spiker, Donna; Lotspeich, Linda J; Dimiceli, Sue et al. (2002) Behavioral phenotypic variation in autism multiplex families: evidence for a continuous severity gradient. Am J Med Genet 114:129-36
Spiker, D; Lotspeich, L J; Dimiceli, S et al. (2001) Birth order effects on nonverbal IQ scores in autism multiplex families. J Autism Dev Disord 31:449-60
Salmon, B; Hallmayer, J; Rogers, T et al. (1999) Absence of linkage and linkage disequilibrium to chromosome 15q11-q13 markers in 139 multiplex families with autism. Am J Med Genet 88:551-6
Risch, N; Spiker, D; Lotspeich, L et al. (1999) A genomic screen of autism: evidence for a multilocus etiology. Am J Hum Genet 65:493-507

Showing the most recent 10 out of 58 publications