M3G-Induced Allodynia Spinal Release of Substance P and Glutamate

Elevation in spinal dynorphin content has also been seen in condition of opioid-induced pain state (Vanderah et al., 2000). Although dynorphine was originally identified as an endogenous K-opioid agonist and may act as an endogenous antinociceptive peptide under certain conditions, considerable 

Mechanism of M3G-lnduced Allodynia Spinal Activation of NO/cGMP/PKG Pathway 

Glial cells play an important role in the control of pain in fact, it is known that neuronal plasticity is triggered by many inflammatory mediators and these are mainly produced by glial cells in the central nervous system. Indeed, in the past 

NO has been implicated in mediating the release of neurotransmitter/neuro-modulators such as substance P or glutamate (Meller and Gebhart, 1993). In addition, glial activation and cytokine production are found to be induced by NO (Guo et al., 2007 Holguin et al., 2004). The role of NO in activated astrocyte-induced glial cytokines after i.t. injection of M3G was examined by using the NO synthase inhibitor L-NAME. In mice treated with M3G, L-NAME was also very 

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II. Mechanism of M3G-Induced Allodynia Spinal Release of Substance P and Glutamate... 

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