GalR1 has also been implicated in pain sensation (Bartfai et al. 1993), and galnon acts as a galanin receptor agonist in the spinal cord (Wiesenfeld-Hallin, preliminary results). GalR2 (but not GalR1) mRNA was found to be significantly increased after injury of the facial nerve in an experimental model, and the levels GalR2 mRNA are further elevated in dorsal root ganglia following inflammation (Burazin and Gundlach 1998; Sten Shi et al. 1997). Surprisingly, both GalR2 and GalR1 mRNA is downregulated in dorsal root ganglia after axotomy, where the levels of the endogenous ligand galanin is significantly (10-20-fold) upregulated (Sten Shi etal. 1997). One explanation for this finding could be the presence of additional, yet unidentified, galanin receptor subtype(s) in these neurones.
Was this article helpful?