Project Details
Description
DESCRIPTION This project aims to
address the question whether the elevated levels of glutamate and other
neurotransmitters that have been reported in brain following an ischemic
insult are indeed important in the subsequent cascade of events leading to
cell death or whether they are merely an expression of generalized energy
failure. The studies will examine the temporal pattern of changes in the
extracellular concentration of excitatory amino acids (EAA) and glycine
following episodes of transient global ischemia in rabbits. Microdialysis
will be used to obtain fine resolution measurements of regional brain
tissue concentrations of these transmitter substances. The relationship
between various physiological variables and pharmacological agents thought
to alter neurologic outcome and the release of EEA will be analyzed. These
agents will include NMDA antagonists and adenosine agonists. The results
of these studies will provide a better understanding of the mechanisms of
neurological injury in ischemic hypoxia and will help to resolve some of
the questions regarding the therapeutic benefit of various neuroprotective
agents and interventions.
address the question whether the elevated levels of glutamate and other
neurotransmitters that have been reported in brain following an ischemic
insult are indeed important in the subsequent cascade of events leading to
cell death or whether they are merely an expression of generalized energy
failure. The studies will examine the temporal pattern of changes in the
extracellular concentration of excitatory amino acids (EAA) and glycine
following episodes of transient global ischemia in rabbits. Microdialysis
will be used to obtain fine resolution measurements of regional brain
tissue concentrations of these transmitter substances. The relationship
between various physiological variables and pharmacological agents thought
to alter neurologic outcome and the release of EEA will be analyzed. These
agents will include NMDA antagonists and adenosine agonists. The results
of these studies will provide a better understanding of the mechanisms of
neurological injury in ischemic hypoxia and will help to resolve some of
the questions regarding the therapeutic benefit of various neuroprotective
agents and interventions.
Status | Finished |
---|---|
Effective start/end date | 5/1/91 → 11/30/01 |
Funding
- National Institutes of Health: $186,838.00
- National Institutes of Health: $247,101.00
- National Institutes of Health: $232,917.00
ASJC
- Medicine(all)
- Neuroscience(all)
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