EXPRESSION OF CHOLINE-ACETYLTRANSFERASE AND NERVE GROWTH-FACTOR RECEPTOR WITHIN HYPOGLOSSAL MOTONEURONS FOLLOWING NERVE INJURY

In the present study we employed light microscopic immunocytochemical techniques in order to investigate the temporal response of choline acetyltransferase (ChAT) and nerve growth factor receptor (NGFr) within hypoglossal motoneurons following unilateral transection or crushing of the XII nerve or after intraneural injections of ricin into the nerve. In control rats (i.e., sham operated) virtually all the motoneurons of the XII nucleus displayed intense immunolabeling for ChAT and were devoid of NGFr immunoreactivity. As early as 3 days post-operative the intensity and the number of ChAT-labeled neurons were reduced on the axotomized side compared to the non-lesioned side. This decrease was maximal approximately two weeks post-operative when virtually no ChAT-labeled cells were present on the lesioned side. In contrast, no loss of hypoglossal neurons was found using Nissl stains. This absence of ChAT immunolabeling persisted for several days, yet by 30 days many of the motoneurons had begun to re-express the enzyme. In contrast to the decrease in ChAT immunoreactivity, transection of the XII nerve also resulted in the expression of NGFr immunoreactivity within the lesioned motoneurons. This response was detected as early as one day post-operatively and continued throughout all time points thus far examined including times after many of the motoneurons had begun to re-express ChAT. Crushing of the XII nerve effected the expression of ChAT and NGFr in a manner comparable to, yet less intense than, that observed following transection. Ricin injected directly into the XII nerve resulted in the loss of hypoglossal motoneurons as demonstrated both in immunohistochemical and Nissl-stained tissue preparations. The cell loss was readily apparent 3 days post-operatively, and ChAT immunoreactivity permanently disappeared. NGFr immunolabeling was seen only in scattered surviving neurons but not in ricin poisoned cells. The possible mechanisms underlying the differential expression of ChAT and NGFr are discussed.