Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair.

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.

Rapid, effective, and long-lasting behavioral recovery produced by microsutures, methylene blue, and polyethylene glycol after completely cutting rat sciatic nerves.

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.

Pathways for plasmalemmal repair mediated by PKA, Epac, and cytosolic oxidation in rat B104 cells in vitro and rat sciatic axons ex vivo.

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.

Further investigation of preoperative overtraining, visual cortex lesions and black-white discrimination by the rat.

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.

Delayed response, preoperative overtraining, and prefrontal lesions in the rat.

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.