Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08NS001630-04
Application #
2259620
Study Section
NST-2 Subcommittee (NST)
Project Start
1993-06-01
Project End
1998-05-31
Budget Start
1996-06-01
Budget End
1997-05-31
Support Year
4
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
University of Chicago
Department
Neurology
Type
Schools of Medicine
DUNS #
225410919
City
Chicago
State
IL
Country
United States
Zip Code
60637

  Publications

Brorson, J R; Schumacker, P T; Zhang, H (1999) Nitric oxide acutely inhibits neuronal energy production. The Committees on Neurobiology and Cell Physiology. J Neurosci 19:147-58
Brorson, J R; Zhang, H (1997) Disrupted [Ca2+]i homeostasis contributes to the toxicity of nitric oxide in cultured hippocampal neurons. J Neurochem 69:1882-9
Brorson, J R; Sulit, R A; Zhang, H (1997) Nitric oxide disrupts Ca2+ homeostasis in hippocampal neurons. J Neurochem 68:95-105
Brorson, J R; Marcuccilli, C J; Miller, R J (1995) Delayed antagonism of calpain reduces excitotoxicity in cultured neurons. Stroke 26:1259-66;discussion 1267
Zhang, H; Weir, B; Marton, L S et al. (1995) Mechanisms of hemolysate-induced [Ca2+]i elevation in cerebral smooth muscle cells. Am J Physiol 269:H1874-90
Brorson, J R; Manzolillo, P A; Gibbons, S J et al. (1995) AMPA receptor desensitization predicts the selective vulnerability of cerebellar Purkinje cells to excitotoxicity. J Neurosci 15:4515-24
Brorson, J R; Bindokas, V P; Iwama, T et al. (1995) The Ca2+ influx induced by beta-amyloid peptide 25-35 in cultured hippocampal neurons results from network excitation. J Neurobiol 26:325-38