Regulation of galanin and galanin receptor 2 expression by capsaicin in primary cultured dorsal root ganglion neurons

Abstract

Galanin is a 29-amino-acid neuropeptide expressed in dorsal root ganglion (DRG) neurons which is thought to play a role in modulation of nociception in neuropathic states. Activation of galanin receptor 2 (GalR2) plays a pronociceptive role and enhances capsaicin-induced nociception in the periphery. GalR2 and vanilloid receptor 1 (VR1) are co-expressed in DRG neurons. Capsaicin evokes acute pain via activation of VR1 expressed in primary sensory neurons. It is not known to what extent galanin and its receptor GalR2 expression is regulated by capsaicin in DRG neurons. Effects of acute (4 h) or chronic (4 d) treatment with capsaicin at different concentrations (0.01, 0.1, 1 micromol/L) on galanin and GalR2 expression in primary cultured DRG neurons were investigated in the present study. Our results showed that acute exposure of high concentration capsaicin (1 micromol/L) increased galanin expression, whereas chronic exposure of low concentration capsaicin (0.01, 0.1 micromol/L) promoted galanin expression. Only chronic exposure of 0.1 micromol/L concentration capsaicin could elevate GalR2 expression, whereas capsaicin did not have this effect at any other conditions in this experiment. These results indicated that certain concentrations or exposure time of capsaicin stimulation may be relevant to upregulation of galanin and its receptor GalR2 expression in DRG cultures suggesting a response to peripheral neuronal stimulation. And also, capsaicin-induced GalR2 expression may be also modulated by capsaicin-induced galanin expression. The possible significance of the neurotransmission of nociceptive information involved in galanin or GalR2 expression caused by capsaicin is still to be clarified.

Effects of Alpha 1- and Alpha 2-Adrenoreceptor Stimulation on Galanin mRNA Expression in Primary Cultured Superior Cervical Ganglion Neurons

“…In the present study, upregulation or downregulation of Gal mRNA expression stimulated by distinct adrenoreceptors in cultured SCG neurons implicated that Gal may also involved in modulation of responses in peripheral nerve fi bers. The evidence has accumulated that Gal is involved in nociception and expressed in both DRG neurons and SCG neurons (Holmberg et al, 2005;Liu and Li, 2008). Sympathetically-maintained pain is thought to be the result of an injury induced coupling between the sympathetic postganglionic neurons and primary afferent nociceptors (Gold et al, 1997).…”

Elevated galanin receptor type 2 primarily contributes to mechanical hypersensitivity after median nerve injury

“…Following sciatic nerve injury, galanin is upregulated in lumbar DRG neurons [ 19 , 22 – 24 ]. Both pro- and anti-nociceptive effects have been attributed to galanin, probably related to the activation of different receptors [ 25 , 26 ]. In fact, three galanin receptors (GalR) have been cloned so far: GalR1, GalR2, and GalR3 [ 23 ].…”