Publications by authors named "WILCOTT R"

To survive, cells must rapidly repair (seal) plasmalemmal damage. Cytosolic oxidation has been shown to increase cell survival in some cases and produce cell death in other protocols. An antioxidant (melatonin; Mel) has been reported to decrease the probability of sealing plasmalemmal damage.

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Behavioral function lost in mammals (including humans) after peripheral nerve severance is slowly (weeks to years) and often poorly restored by 1-2-mm/day, nonspecifically directed outgrowths from proximal axonal stumps. To survive, proximal stumps must quickly repair (seal) plasmalemmal damage. We report that, after complete cut- or crush-severance of rat sciatic nerves, morphological continuity, action potential conduction, and behavioral functions can be consistently (>98% of trials), rapidly (minutes to days), dramatically (70-85% recovery), and chronically restored and some Wallerian degeneration prevented.

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Plasmalemmal repair (sealing) is necessary for survival of damaged eukaryotic cells. Ca(2+) influx through plasmalemmal disruptions activates pathways that initiate sealing, which is commonly assessed by exclusion of extracellular dye. These sealing pathways include PKA, Epac, and cytosolic oxidation.

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Preoperative overtraining can improve retention after brain lesions. However, studies of effects of overtraining on relearning of a black-white discrimination after visual cortex lesions in the rat have obtained conflicting results. Another experiment was done on this problem.

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An earlier study in this laboratory found that preoperative overtraining improved retention of a delayed alternation task after prefrontal lesions in the rat. In this study, however, it was found that preoperative overtraining did not improve performance of the rat in a delayed response task following prefrontal lesions. These results support the hypothesis that preoperative overtraining can improve postoperative performance only when postoperative recovery is ordinarily present, as it is with delayed alternation.

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It was found that during low-frequency electrical stimulation of either the septal medial or lateral nucleus suppression of an operant response can occur without a stimulation-induced reward or aversion effect. Further, the behavior of rats during response suppression appeared to be the same as when they stopped responding without stimulation. These observations suggest that response suppression to low-frequency stimulation of the septal area is not due to production of some disruptive factor.

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Electrical stimulation in the bulbar reticular formation will produce response suppression that is observably the same as that produced by stimulation in the prefrontal cortex. This includes suppression of bar-pressing for food and running in an activity wheel, but no suppression of approach and eating of food or general activity. These results, together with previous research, support the hypothesis that this inhibitory influence of the prefrontal cortex is mediated through the bulbar reticular formation.

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Parts of the rat's neocortex were mapped for sites where electrical stimulation, square waves at 10/sec, will suppress a bar-press response for food. Effective sites were found in the frontal pole and over most of the frontal dorsolateral cortex. Within these regions the strongest inhibitory influences were at sites in the frontal pole and adjacent frontal cortex, and at sites along the midline.

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