Nerve growth factor and norepinephrine regulate galanin expression in primary cultures of dorsal root ganglion neurons

Nerve growth factor (NGF) is a major regulator of inflammatory and homeostatic pain states, influencing both sensory neuron phenotype and physiologic responses (Petruska & Mendell, 2004). It is known that NGF is one of the well characterized regulators of galanin expression (Thippeswamy et al., 2007). NGF regulates galanin expression occurring in dorsal root ganglion (DRG) cells after intravesical resiniferatoxin (RTX) application (Avelino et al., 2002). NGF deprivation can induce galanin expression in DRG neurons (Kato et al., 2002; Thippeswamy et al., 2007). Axonal transection of adult sensory neurons leads to a decrease in the content of target-derived NGF and to dramatic changes in the expression of several neuropeptides including galanin (Shadiack et al., 2001). The 29-30 amino acid neuropeptide galanin is present in a small population of DRG neurons under normal conditions but is strongly up-regulated after nerve injury (Zvarova et al., 2004; Wilson-Gerwing & Verge, 2006). Axotomy of sensory neurons in DRG increases protein and mRNA levels for galanin (Shadiack et al., 2001). Systemic or topical administration of vanilloid substances has been shown to up-regulate galanin in primary sensory neurons (Avelino et al., 2002). There is evidence that this up-regulated galanin has trophic actions, for example promoting neurite outgrowth as well as influencing pain processing (Landry et al., 2005). Furthermore, galanin is recognized as one of the DRG injury markers (Shortland et al., 2006). Norepinephrine (NE) is a classical neurotransmitter which plays a key role in the neuronal response to environmental influences through activation of