Violeta
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I am pretty sure this study should supply me with enough information to figure out how to relieve postherpetic neuralgia. But I don't understand very much of it. If anyone has input, I would appreciate it.
Involvement of Tyr1472 Phosphorylation of NMDA Receptor NR2B Subunit in Postherpetic Neuralgia in Model Mice
Sawako Unezaki†, Atsushi Sasaki†, Tamaki Mabuchi, ...
https://journals.sagepub.com/doi/full/10.1186/1744-8069-8-59
Based on data they had obtained by using this mouse model, Sasaki et al. recently suggested that herpetic and postherpetic allodynia are mediated by nitric oxide (NO) in the dorsal horn and that inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) are responsible for herpetic and postherpetic allodynia, respectively. Many studies including ours have demonstrated that activation of the NMDA subtype of glutamate receptors and subsequent NO production is a fundamental event in neurotransmission and synaptic plasticity in pain transmission in the spinal cord. Garry et al. demonstrated that the VZV-induced pain state is attenuated by intrathecal administration of an NMDA receptor antagonist and that the profile of VZV infection-induced phenotype changes in dorsal root ganglia (DRGs) are similar to those in other neuropathic pain models. We showed earlier that an increase in nNOS activity associated with Tyr1472 phosphorylation of the NR2B subunit in the superficial dorsal horn of the spinal cord reflects the neuropathic pain state even 1 week after nerve injury
Involvement of Tyr1472 Phosphorylation of NMDA Receptor NR2B Subunit in Postherpetic Neuralgia in Model Mice
Sawako Unezaki†, Atsushi Sasaki†, Tamaki Mabuchi, ...
https://journals.sagepub.com/doi/full/10.1186/1744-8069-8-59
Based on data they had obtained by using this mouse model, Sasaki et al. recently suggested that herpetic and postherpetic allodynia are mediated by nitric oxide (NO) in the dorsal horn and that inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS) are responsible for herpetic and postherpetic allodynia, respectively. Many studies including ours have demonstrated that activation of the NMDA subtype of glutamate receptors and subsequent NO production is a fundamental event in neurotransmission and synaptic plasticity in pain transmission in the spinal cord. Garry et al. demonstrated that the VZV-induced pain state is attenuated by intrathecal administration of an NMDA receptor antagonist and that the profile of VZV infection-induced phenotype changes in dorsal root ganglia (DRGs) are similar to those in other neuropathic pain models. We showed earlier that an increase in nNOS activity associated with Tyr1472 phosphorylation of the NR2B subunit in the superficial dorsal horn of the spinal cord reflects the neuropathic pain state even 1 week after nerve injury