Abstract

Dr. Rasenick's research centers around the question of regulation of neurotransmitter responsiveness with a specific focus upon the adenylate cyclase system, and the aspects of the neuronal adenylate cyclase systems which are distinct from those found in other tissues. Specific aspects of this proposal involve probing the link between the GTP-binding proteins responsible for stimulation or inhibition of adenylate cyclase and components of the neuronal cytoskeleton. A new GTP-binding protein which may be unique to neurons has been discovered and experiments to purify and characterize this protein are proposed. Functional reconstitution studies between resolved adenylate cyclase components and cultured neural cells, using a newly developed permeabilized cell adenylate cyclase assay are also proposed. Finally, several collaborative studies including some concerning antidepressants and the adenylate cyclase system have been proposed.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Scientist Development Award - Research (K02)
Project #
5K02MH000699-05
Application #
3070106
Study Section
Research Scientist Development Review Committee (MHK)
Project Start
1987-08-01
Project End
1992-07-31
Budget Start
1991-08-01
Budget End
1992-07-31
Support Year
5
Fiscal Year
1991
Total Cost
Indirect Cost

  Institution

Name
University of Illinois at Chicago
Department
Type
Schools of Medicine
DUNS #
121911077
City
Chicago
State
IL
Country
United States
Zip Code
60612

  Publications

Rasenick, M M; Chaney, K A; Chen, J (1996) G protein-mediated signal transduction as a target of antidepressant and antibipolar drug action: evidence from model systems. J Clin Psychiatry 57 Suppl 13:49-55;discussion 56-8
Chen, J; Rasenick, M M (1995) Chronic treatment of C6 glioma cells with antidepressant drugs increases functional coupling between a G protein (Gs) and adenylyl cyclase. J Neurochem 64:724-32
Chen, J; Rasenick, M M (1995) Chronic antidepressant treatment facilitates G protein activation of adenylyl cyclase without altering G protein content. J Pharmacol Exp Ther 275:509-17
Rasenick, M M; Watanabe, M; Lazarevic, M B et al. (1994) Synthetic peptides as probes for G protein function. Carboxyl-terminal G alpha s peptides mimic Gs and evoke high affinity agonist binding to beta-adrenergic receptors. J Biol Chem 269:21519-25
Popova, J S; Johnson, G L; Rasenick, M M (1994) Chimeric G alpha s/G alpha i2 proteins define domains on G alpha s that interact with tubulin for beta-adrenergic activation of adenylyl cyclase. J Biol Chem 269:21748-54
Roychowdhury, S; Rasenick, M M (1994) Tubulin-G protein association stabilizes GTP binding and activates GTPase: cytoskeletal participation in neuronal signal transduction. Biochemistry 33:9800-5
Roychowdhury, S; Wang, N; Rasenick, M M (1993) G protein binding and G protein activation by nucleotide transfer involve distinct domains on tubulin: regulation of signal transduction by cytoskeletal elements. Biochemistry 32:4955-61
Lazarevic, M B; Yan, K; Swedler, W I et al. (1992) Effect of gold compounds on the activity of adenylyl cyclase in human lymphocyte membranes. Arthritis Rheum 35:857-64
Wang, N; Rasenick, M M (1991) Tubulin-G protein interactions involve microtubule polymerization domains. Biochemistry 30:10957-65
Ozawa, H; Rasenick, M M (1991) Chronic electroconvulsive treatment augments coupling of the GTP-binding protein Gs to the catalytic moiety of adenylyl cyclase in a manner similar to that seen with chronic antidepressant drugs. J Neurochem 56:330-8

Showing the most recent 10 out of 16 publications