TIME COURSE AND DISTRIBUTION OF MOTONEURONAL LOSS IN THE DORSAL MOTOR VAGAL NUCLEUS OF GUINEA-PIG AFTER CERVICAL VAGOTOMY

Cells in the dorsal motor vagal nucleus (DMVN) of the adult guinea pig were counted at different times after unilateral cervical section of the vagus nerve. The counts were made from serial 30 .mu.m coronal sections throughout the DMVN in normal and operated animals. There are three types of cells in the DMVN of guinea pig: medium-sized motoneurons that are retrogradely filled by HRP from the site of the vagotomy, small neurons, and glial cells. An interesting observation was a change in distribution of cells in the DMVN with age in unoperated guinea pigs. Following vagotomy degeneration was seen only in the motoneurons. Disappearance of motoneurons was slow and only 27% were present after 1 year. During that time the decrease in the total number of motoneurons was exponential with a time constant of 8.6 months, but degeneration in different parts of the nucleus was not uniform. Thirty-four percent of motoneurons in the caudal area of DMVN disappeared in the first month after vagotomy, while the rostral area was almost unchanged. The rostral area, however, showed rapid degeneration between 3 and 6 months after vagotomy. The central part of the nucleus degenerated at a constant rate between those of the rostral and caudal regions. At the end of 1 year, cell loss in all parts of the nucleus was approximately equal. Surviving motoneurons showed morphological changes: rounding of the soma, continuous reduction of the cell volume, and shrinkage of the nucleus. Occasional abnormal forms showing vacuolization or invaginated nuclei were seen. Calculations show that the process of degeneration lasts 25 days on the average. The marked degeneration found in dorsal vagal motoneurons, in contrast to recovery form axotomy in somatic motoneurons, is similar to that found in intrinsic neurons of the central nervous system. The slow and continuous time course of disappearance of motoneurons after vagotomy, however, is exceptional. It is reasonable to postulate that the increased vulnerability of these motoneurons may be sufficient to result in degeneration in response to what are normally nonpathological metabolic demands.