COLOCALIZATION AND COVARIATION OF C-JUN TRANSCRIPTION FACTOR WITH GALANIN IN PRIMARY AFFERENT NEURONS AND WITH CGRP IN SPINAL MOTONEURONS FOLLOWING TRANSECTION OF RAT SCIATIC-NERVE

The expression of galanin (GAL) in L5 dorsal root ganglia (DRG) and calcitonin gene-related peptide (CGRP) in motoneurons (MN) of lumbar spinal cord and their colocalisation with the nuclear c-JUN protein was investigated by immunocytochemistry following transection of rat sciatic nerve. Expression of c-JUN in L5 DRG neurons increased 10 h following transection. Between 24 h and 10 days 64%-72% of all neurons were labelled. After 50 and 150 days, the end of the observation period, 62% and 27%, respectively, of neurons were labelled by c-JUN. Expression of GAL started after 24 h, reached a maximum between 2 and 10 days in 40-50% of all neurons and persisted in 37% up to 50 days. After 150 days, GAL-IR had returned to basal levels. Between. 24 h and 150 days, 75%-86% of all GAL positive neurons showed a nuclear c-JUN immunoreactivity, the maximal number was visible between 2 and 10 days. After 30 days, small diameter neurons showed a slightly increased colocalisation of GAL and c-JUN compared to large diameter neurons. In motoneurons (MN) of lumbar spinal cord of untreated rats, c-JUN was predominantly visible in small diameter MN. The number of c-JUN labelled MN raised 15 h following sciatic nerve transection in both small and large diameter MN. It reached its maximum after 2 days and declined after 40 days. CGRP showed basal expression exclusively in large MN. Its expression raised after 20 h, showed a maximum after 48 h and returned to control levels after 20 days. The increase of CGRP was restricted to large MN. All MN which showed an intense distinctly suprabasal CGRP-IR also showed an intense nuclear labelling of c-JUN. The close temporo-spatial relationship between the expression of c-JUN and of the neuropeptides GAL and CGRP suggests that c-JUN could be involved in the transcriptional control of genes encoding for GAL and CGRP in lesioned neurons.