Postganglionic sympathetic efferents play a critical role in several types of pathological pain

Postganglionic sympathetic efferents play a critical role in several types of pathological pain (Gibbs et al., 2008; Jänig and McLachlan, 1994; Jänig et al., 1996; Raja, 1995). For example, sympathetic stimulation may excite sensory neurons in animals with inflamed peripheral tissue or after peripheral nerve injury (Devor et al., 1994; Sato and Kumazawa, 1996; Sato and Perl, 1991). Sympathectomy relieves hyperalgesic and allodynic behaviors in several pathological pain models (Kim et al., 1993; Kinnman and Levine, 1995; Malmberg and Basbaum, 1998). Clinical observations and experimental studies suggest that a crosstalk between sympathetic efferents and sensitized primary afferent nociceptors is produced by the release of norepinephrine, adenosine 5′-triphosphate (ATP) and/or neuropeptide Y from sympathetic efferents onto dorsal root ganglion (DRG) neurons (Chung et al., 1996; Devor et al., 1994), at the site of nerve injury (Devor and Seltzer, 1999) and in the skin (Lin et al., 2003,2004; Sato and Perl, 1991).

Many studies reveal that neurogenic inflammation and the resulting pain induced by intradermal injection of capsaicin (CAP) are sympathetically dependent (Coderre et al., 1989; Lin et al., 2003,2004; Ren et al., 2005,2006). Activation of transient receptor potential vanilloid-1 (TRPV1) receptors in primary afferent nociceptive neurons and their axons evoked by CAP injection produces an efferent function that initiates neurogenic inflammation (Kessler et al., 1999; Szolcsanyi, 1996,2004) by the release of neuropeptides from the nociceptors (Garcia-Nicas et al., 2001; Li et al., 2008; Lin et al., 2007). We proposed in our previous studies that neurogenic inflammation is likely to be sympathetically-mediated by influencing the sensitivity of primary afferent nociceptive neurons and/or their terminals (Ren et al., 2005,2006). However, no direct evidence has so far been provided to show if this process is done by modulation of TRPV1receptors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824038/

Exp Neurol. Author manuscript; available in PMC Mar 1, 2011.

Published in final edited form as:

Exp Neurol. Mar 2010; 222(1): 93–107.

Published online Dec 28, 2009. doi:  10.1016/j.expneurol.2009.12.011