Axon reaction in hypoglossal and dorsal motor vagal neurons of adult rat: Incorporation of [ 3H]leucine

Pairs of adult rats received [ 3H]leucine (i.p., 5 μCi/g body weight) 0.25, 1, and 16 h before killing and zero (unoperated control animals) and 1 to 164 days after unilateral cervical vagotomy and hypoglossal neurotomy. Grain counts and morphometric measurements were made on axotomized and uninjure...

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Veröffentlicht in:Exp. Neurol.; (United States) 1984-07, Vol.85 (1), p.139-151
Hauptverfasser: Aldskogius, Hakan, Barron, Kevin D., Regal, Ronald
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Sprache:eng
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Zusammenfassung:Pairs of adult rats received [ 3H]leucine (i.p., 5 μCi/g body weight) 0.25, 1, and 16 h before killing and zero (unoperated control animals) and 1 to 164 days after unilateral cervical vagotomy and hypoglossal neurotomy. Grain counts and morphometric measurements were made on axotomized and uninjured neurons in histoautoradiographs of the medullary nuclei. Axotomized hypoglossal neurons, which largely survive the injury, both enlarged and incorporated increased amounts of tritiated leucine at each labeling interval, 3 through 28 days postoperatively. In the vagal dorsal motor nucleus (DMN), axotomized cells, which frequently die after neurotomy, enlarged slightly through 28 days postoperatively, then atrophied; DMN neurons increased amino acid uptake for a shorter period (days 7 through 14) than hypoglossal neurons. This increase achieved statistical significance only when the labeling intervals were 0.25 or 1.0 h. Neurons of the DMN contralateral to vagotomy also enlarged. Axotomized DMN neurons did not sustain increased protein synthesis as long as their hypoglossal counterparts and seemed to fail to increase synthesis of structural protein with long half-lives (16-h labeling interval). The frequently necrobiotic response of axotomized DMN neurons may relate to these phenomena. From these and earlier results, we conclude that axon reaction appears to differ fundamentally in peripheral and central neurons. This difference may have significance for research on regeneration in the central nervous system.
ISSN:0014-4886
1090-2430
DOI:10.1016/0014-4886(84)90168-7