Specific temporal and spatial distribution of JUN, FOS, and KROX‐24 proteins in spinal neurons following noxious transsynaptic stimulation

Abstract

We present the first comparative investigation of the basal and transsynaptically induced expression of c-JUN, JUN B, JUN D, c-FOS, FOS B, and KROX-24 proteins in the spinal cord, using immunocytochemistry with specific antibodies. We demonstrate that electrical stimulation of the sciatic nerve at A delta/C-fiber (not A alpha/beta-fiber) intensity strongly induces the expression of these immediate-early gene-encoded proteins. Basal immunoreactivity was found for c-JUN in motoneurons, for JUN D in almost every cell of the gray matter, and for KROX-24 in the superficial dorsal horn. One hour after electrical stimulation of the sciatic nerve at A delta/C-fiber intensity, expression of all proteins except JUN D reached its maximum. Initially immunoreactivity was restricted to the ipsilateral dorsal horn, but after 4 hours appeared contralaterally. Expression of JUN D was increased only after 4 hours. Within the dorsal horn, the expression of c-JUN, JUN B, FOS B, and KROX-24 was mainly restricted to the superficial layers. Immunoreactivity decreased to basal levels between 8 and 16 hours. c-FOS and JUN D were expressed in both the superficial and deep dorsal horn; in the latter, c-FOS and JUN D persisted longer. Induced JUN D was present the longest and was still visible after 32 hours. In motoneurons of the ipsilateral ventral horn, c-JUN, JUN D, and c-FOS appeared after 8 hours. Surgical exposure of the sciatic nerve evoked a strikingly prolonged expression of all proteins compared to that following electrical stimulation of the sciatic nerve. Our results demonstrate that stimulation of nociceptive A delta- and C-fibers induces early and late expression of proteins encoded by immediate-early genes with a specific temporal and spatial distribution of the expression of each protein. Furthermore, the extent of protein expression reflects the intensity of noxious stimulation.

Gap‐43 immunoreactivity and axon regeneration in retinal ganglion cells of the rat

“…They were exposed to monoclonal antibody against GAP-43 (Schreyer and Skene, 1991; kindly provided by P. Skene) overnight at 4°C (dilution 1: 100.000), and after rinses in PBS incubated in polyclonal anti-c-JUN antibodies (Herdegen et al, 1993; dilution I: 1000) for 36 h at 4oe. The specificity of polyclonaJ antibodies against c-JUN has been shown previously by immunoprecipitation and in vivo preabsorption experiments (Herdegen, et al, 1991;Kovary and Bravo, 1991). Secondary antibodies were fluorescein isothiocyanate-coupled goat anti-rabbit and rhodamine isothiocyanate-coupled goat anti-mouse antibodies (I :200, Dianova) applied for 2 h at room temperature.…”

Neuronal regulation of c-fos, c-jun, and junB immediate-early genes in rat adrenal medulla

“…A rabbit polyclonal antiserum generated against amino acids 128-152 of the rat Fos (Young et al, 1991) was generously donated by Dr. Michael Iadarola (NIH, Bethesda, MA). The Jun (607/6) and JunB (725/5) antibodies were raised in rabbits against amino acids SO-334 and 46-344, respectively (Herdegen et al, 1991;Kovary and Bravo. 1991).…”

Reduction of carrageenin oedema and the associated c‐Fos expression in the rat lumbar spinal cord by nitric oxide synthase inhibitor

“…Since spinal c-Fos expression is strongly associated with noxious spinal transmission (see references in Herdegen et al, 1991;Abbadie et al, 1994;Zieglgansberger & Tolle, 1993), the ability of L-NAME to reduce such an expression strongly implies a pro-nociceptive role of NO. In this respect it must be emphasised that L-NAME reduced c-Fos expression in the superficial and deep laminae neurones of the dorsal horn, the same laminae in which noxiously evoked neurones are located (Besson & Chaouch, 1987;Willis & Coggeshall, 1991).…”