Effect of NGF treatment on outcome measures in a rat model of middle cerebral artery occlusion

T. A. Kent, M. Quast, G. Taglialatela, C. Rea, J. Wei, Z. Tao, Jose R Perez-Polo

    Research output: Contribution to journalArticlepeer-review

    15 Scopus citations


    Ischemic insults to the brain result in a time-dependent increase in neuronal death that is responsible for some of the functional deficits associated with stroke. Our working hypothesis is that ischemia results in a prompt depletion of high energy phosphate species resulting in decreased pH and glutathione levels in brain in a temporal and spatial pattern that disrupts nerve growth factor homeostasis and increases neuronal apoptosis. Here we show hemispheric depletion of active phosphate species after ischemia. Also, we observed that the striatum is an early target for oxidative stress that is followed by energy metabolic impairment and altered neurotrophin levels that were detected by noninvasive magnetic resonance imaging (MRI) measurements of cytotoxicity and conventional biochemical determinations of apoptosis, glutathione, and nerve growth factor (NGF) protein levels in a pattern distinct from that observed in the hippocampus. Furthermore, early assessment of intracellular pH by 31P-magnetic resonance spectroscopy (31P-MRS) was a predictor of later infarct development as determined by MRI. We also show that pretreatment with pharmacological doses of NGF did not have overall significant beneficial consequences on irreversible ischemia in an intraluminal unilateral irreversible model of stroke in rat brain.

    Original languageEnglish (US)
    Pages (from-to)357-369
    Number of pages13
    JournalJournal of Neuroscience Research
    Issue number3
    StatePublished - Feb 1 1999


    • Glutathione
    • Magnetic resonance imaging
    • Middle cerebral artery occlusion
    • Nerve growth factor
    • Nuclear magnetic resonance
    • Stroke

    ASJC Scopus subject areas

    • Cellular and Molecular Neuroscience


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