Ca2+ and Anoxic Damage in the Hippocampal Slice
{'Code': '08090200', 'Directorate': {'Abbreviation': 'BIO', 'LongName': 'Direct For Biological Sciences'}, 'Division': {'Abbreviation': 'IOS', 'LongName': 'Division Of Integrative Organismal Systems'}}
{'SignBlockName': 'Stacy Springer', 'PO_EMAI': None, 'PO_PHON': None}
The general problem addressed in this research is the                           irreversible brain damage resulting from short exposures to                     anoxia/ischemia.  The problem will be studied in a model system,                the rate hippocampal slice preparation.  Irreversible damage in                 this system is the permanent blockage of synaptic transmission                  following 10 minutes oxygen deprivation.  The research will                     address two basic questions about the mechanism of this permanent               damage: 1) Is increased cytosolic calcium during anoxia, a major                initiator of the damage?  and 2) How does glutamate or aspartate                release during anoxia contribute to causing the damage?  With                   regard to the last question, the work is designed to test the                   hypothesis that this amino-acid toxicity during anoxia occurs                   because of binding to NMA receptors and the subsequent release of               calcium from intracellular organelles, probably mediated by                     increased production of inositol-3-phosphate.                                                                                                                   The studies address the two questions, and the hypothesis,                      largely by estimation of changes in cytosolic calcium, made by                  measurements to tissue regions which are damaged and by                         correlating damage with changes in calcium and with changes in                  IP3 in different conditions.  Significant advances should be made               towards dealing with these two very important issues.
{'FirstName': 'Peter', 'LastName': 'Lipton', 'PI_MID_INIT': None, 'PI_SUFX_NAME': None, 'PI_FULL_NAME': 'Peter Lipton', 'EmailAddress': 'plipton@wisc.edu', 'NSF_ID': '000150243', 'StartDate': '01/01/1988', 'EndDate': None, 'RoleCode': 'Principal Investigator'}
{'Name': 'University of Wisconsin-Madison', 'CityName': 'MADISON', 'ZipCode': '537151218', 'PhoneNumber': '6082623822', 'StreetAddress': '21 North Park Street', 'StreetAddress2': 'Suite 6301', 'CountryName': 'United States', 'StateName': 'Wisconsin', 'StateCode': 'WI', 'CONGRESSDISTRICT': '02', 'CONGRESS_DISTRICT_ORG': 'WI02', 'ORG_DUNS_NUM': '161202122', 'ORG_LGL_BUS_NAME': 'UNIVERSITY OF WISCONSIN SYSTEM', 'ORG_PRNT_DUNS_NUM': '041188822'}
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[{'Code': '1192', 'Text': 'NEURONAL AND GLIAL MECHANISMS'}, {'Code': '9120', 'Text': 'CROSS-DIRECTORATE PROGRAMS'}]
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