Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Specialized Center (P50)
Project #
3P50MH049176-08S1
Application #
6216675
Study Section
Project Start
1999-09-10
Project End
2000-08-30
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
8
Fiscal Year
1999
Total Cost
Indirect Cost
Name
California Institute of Technology
Department
Type
DUNS #
078731668
City
Pasadena
State
CA
Country
United States
Zip Code
91125
Sokolova, Irina V; Lester, Henry A; Davidson, Norman (2006) Postsynaptic mechanisms are essential for forskolin-induced potentiation of synaptic transmission. J Neurophysiol 95:2570-9
Schwarz, Johannes; Schwarz, Sigrid C; Dorigo, Oliver et al. (2006) Enhanced expression of hypersensitive alpha4* nAChR in adult mice increases the loss of midbrain dopaminergic neurons. FASEB J 20:935-46
Chiu, Chi-Sung; Brickley, Stephen; Jensen, Kimmo et al. (2005) GABA transporter deficiency causes tremor, ataxia, nervousness, and increased GABA-induced tonic conductance in cerebellum. J Neurosci 25:3234-45
Kovoor, Abraham; Seyffarth, Petra; Ebert, Jana et al. (2005) D2 dopamine receptors colocalize regulator of G-protein signaling 9-2 (RGS9-2) via the RGS9 DEP domain, and RGS9 knock-out mice develop dyskinesias associated with dopamine pathways. J Neurosci 25:2157-65
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Fonck, Carlos; Nashmi, Raad; Deshpande, Purnima et al. (2003) Increased sensitivity to agonist-induced seizures, straub tail, and hippocampal theta rhythm in knock-in mice carrying hypersensitive alpha 4 nicotinic receptors. J Neurosci 23:2582-90
Jensen, Kimmo; Chiu, Chi-Sung; Sokolova, Irina et al. (2003) GABA transporter-1 (GAT1)-deficient mice: differential tonic activation of GABAA versus GABAB receptors in the hippocampus. J Neurophysiol 90:2690-701
Yu, Tzu-Ping; Lester, Henry A; Davidson, Norman (2003) Requirement of a critical period of GABAergic receptor blockade for induction of a cAMP-mediated long-term depression at CA3-CA1 synapses. Synapse 49:12-9
Slimko, Eric M; Lester, Henry A (2003) Codon optimization of Caenorhabditis elegans GluCl ion channel genes for mammalian cells dramatically improves expression levels. J Neurosci Methods 124:75-81

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