Effects of Vincristine on the CNS

It is well known that signal transduction of pain initiates in primary afferent neurons and transmits to the dorsal horn of the spinal cord (Scholz and Woolf, 2002). Signal transduction in the spinal cord is important for nociception, but dynamic change (i.e., central sensitization) and neuronal plasticity associated with glial activation also have important roles in neuropathic pain (Inoue et al., 2007 Tsuda et al., 2005). Central sensitization was demonstrated in neuropathic pain 

There are several reports concerning the participation of microglia and astrocyte-derived neurotrophic factors and inflammatory cytokines in neuropathic pain (Coull et al., 2005 Inoue et al., 2007 Scholz and Woolf, 2007). TNF-o was upregulated in the PNS and CNS after nerve injury, and contributed to neuropathic pain (Scholz and Woolf, 2007). The p38 MAP kinase was activated by TNF-a after nerve injury, and elicited neuropathic pain (Jin et al., 2003 Schafers et al., 2003). These findings were confirmed by studies using neutralizing antibody for TNF-a and p38 MAP kinase inhibitor (Schafers et al., 2003). A local injection of recombinant TNF-a elicited neuropathic-like pain (Wei et al., 2007). These reports indicate that TNF-a signaling has a critical role in the development 

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