The rubrospinal tract (RST) was cut unilaterally at C2-3 segment in 21 rats that were killed 3, 7, 10, 14, 28, 60, and 90 days later. Additionally, 14 rats, killed 14 or 28 days after lesioning, were treated postoperatively by daily intraperitoneal injections of GM1 ganglioside. Six unoperated, untreated rats served as controls. In untreated animals, axotomized neurons of the magnocellular division of the red nucleus (RN) exhibited cytoplasmic, nuclear, and nucleolar atrophy 7-10 days postoperatively. Atrophy progressed through the 90th postoperative day. Regression analyses disclosed a bimodal pattern to cytoplasmic and nucleolar atrophy, with an initial rapid phase changing to a slower but progressive mode from 14 days postoperatively. Nuclear atrophy proceeded in a unimodal manner. GM1 treatment did not affect these atrophic processes. Neuronal loss did not occur in the axotomized RN through the 60th postoperative day. Axotomized neurons of untreated rats showed significant and progressive reductions in mean somal (cytoplasmic) and nucleolar RNA from, respectively, the 7th and 14th postoperative day. GM1 partly prevented these RNA losses. Both in treated and untreated rats, spinal cord lesions contained many axonal sprouts 2 to 4 weeks after surgery, but newly generated axons did not traverse the rostro-caudal extent of any lesion.

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Microspectrophotometric estimates of RNA content and morphometric measurements of cytoplasmic, nuclear and nucleolar areas were made on 30 to 60 motoneurons (somal areas greater than 1000 microns2) ipsilateral and contralateral to brachial plexotomy performed unilaterally on adult cats 2-90 days before sacrifice. Nerve cells of unoperated animals were also assayed. Somal and cytoplasmic areas of axotomized motoneurons were larger than those of the corresponding, contralateral motor nerve cells 4, 6 and 75 days postoperatively. Because of between animal variability, it could not be determined, however, whether this difference was due to an increase in the area of the axotomized motoneurons or to a decrease in the area of the contralateral nerve cells. Nucleolar sizes did not change. In contrast, nuclei of axotomized motoneurons showed a temporary but unequivocal areal decrease. The cytoplasmic RNA content of axotomized motoneurons fell 14-28 days postoperatively but rose thereafter, being increased slightly but significantly 75-90 days after operation. At no postoperative interval, however, did the nucleolar RNA content of the axotomized cells deviate unequivocally from the unoperated or zero day condition. The following points may be emphasized: 1. these results differ from similar measurements of axotomized motoneurons of rodents and lagomorphs; 2. the data do not provide certain evidence of change in either morphometric parameters or RNA content of motoneurons on the side contralateral to surgery, although the possibility of a decrease in the size of these uninjured neurons should be considered; 3. morphometric and RNA measurements on axotomized peripheral (extrinsic) neurons of spinal anterior horn of cat contrast with similar measurements on axotomized central (intrinsic) neurons of cat red nucleus.

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