The permissive role of hyperthermia in the disaggregation of brain polysomes by L-dopa or D-amphetamine.
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Biomedical subjects
T S Nowak
Publications and source records attributed to T S Nowak.
Evidence for the synthesis of tubulin on membrane-bound and free ribosomes from rat forebrain.
Evidence is presented that tubulin is synthesized in cell-free systems derived from rat forebrain containing either membrane-bound or free ribosomes. Both systems were supplemented with saturating amounts of messenger RNA (from either membrane-bound of free ribosomes) and soluble enzyme and initiation factors from whole forebrain. Synthesized products were chracterized by two biochemical purification methods for brain tubulin isolation. These methods of tubulin analysis indicated that both cell free systems synthesized the same relative amounts of tubulin.
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Role of circulatory disturbances in the development of post-ischemic brain edema.
Two post-ischemic circulatory disturbances that play a significant role in pathophysiology of an ischemic lesion are: (1) reactive hyperemia or hyperperfusion and (2) hypoperfusion. The reactive hyperemia promptly follows release of major cerebral artery occlusion, and it is associated with the opening of the blood-brain barrier to serum proteins and ensuing edema. Prevention or reduction of reactive hyperemia results in significant amelioration of edema and the resulting ischemic brain tissue injury. The post-ischemic hypoperfusion, studied in gerbils, develops soon after recirculation and usually lasts up to 6 h. Its relationship to post-ischemic edema is evident in repeated ischemic insults. In these studies, three ischemic insults of 5 min duration when applied at 1 h intervals, i.e., during the period of hypoperfusion, resulted in a cumulative effect, post-ischemic edema and tissue injury becoming considerably more pronounced that those following a single 15 min ischemia. There was no cumulative effect when the ischemic insults were spaced 3 min or longer than 6 h apart. These observations indicate that repeated ischemic insults taking place during the phase of post-ischemic hypoperfusion may significantly increase the development of edema and brain tissue injury.
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Opioid peptide levels in gerbil brain after transient ischemia: lasting depletion of hippocampal dynorphin.
Peptides derived from each of the 3 endogenous opioid precursors were measured in gerbil brain regions at various times after transient bilateral carotid artery occlusion using radioimmunoassays specific for beta-endorphin-, met-enkephalin-, and dynorphin A-related peptides. Lasting changes were observed only in the hippocampus. The most striking effect was on dynorphin A immunoreactivity, which was reduced by 30-40% as early as 1 hour after recirculation and remained at 50% of the control level for at least 1 week. In some experiments dynorphin levels showed a transient recovery at 24 hours. These results demonstrate a unique sensitivity of the dynorphin-containing dentate granule cell-mossy fiber pathway to transient ischemia. Although these cells remain histologically intact, the decrease in dynorphin level precedes and continues during the delayed loss of hippocampal CA1 neurons characteristic of this model and further defines the selective vulnerability of hippocampal circuitry following ischemia. These observations clearly identify the hippocampus as a well-defined brain region in which further studies of the postischemic pathophysiology of endogenous opioid peptides may provide a rational basis for evaluating the place of opiate pharmacology in stroke treatment.
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