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Difference between revisions of "Pain Pathophysiology"
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Some data suggest that, in chronic pain, specific genes involved in apoptosis are active, contributing to critical changes in cell survival and the establishment of chronic pain states <ref>Ham J, Babij C, Whitfield J. Activation of c-Jun N-terminal kinase in dorsal root ganglion neurons following axotomy. J Neurosci 1997; 17: 6464-6472.</ref>. | Some data suggest that, in chronic pain, specific genes involved in apoptosis are active, contributing to critical changes in cell survival and the establishment of chronic pain states <ref>Ham J, Babij C, Whitfield J. Activation of c-Jun N-terminal kinase in dorsal root ganglion neurons following axotomy. J Neurosci 1997; 17: 6464-6472.</ref>. | ||
Following axonal injury, some neurons in the dorsal root ganglia undergo apoptosis, resulting in deafferentation of postsynaptic spinal neurons. These in turn degenerate due to the lack of tonic inhibitory stimulation of apoptosis normally exerted by the presynaptic neuron. The preventive administration of MK-801, a competitive NMDAR antagonist, prevents cell death due to axotomy in nearly all cases <ref>Lopez-Garcia JA, King AE. Neuronal cell death after peripheral nerve injury and the role of NMDAR activation. J Neurosci 1997; 17: 4325-4332.</ref>. | Following axonal injury, some neurons in the dorsal root ganglia undergo apoptosis, resulting in deafferentation of postsynaptic spinal neurons. These in turn degenerate due to the lack of tonic inhibitory stimulation of apoptosis normally exerted by the presynaptic neuron. The preventive administration of MK-801, a competitive NMDAR antagonist, prevents cell death due to axotomy in nearly all cases <ref>Lopez-Garcia JA, King AE. Neuronal cell death after peripheral nerve injury and the role of NMDAR activation. J Neurosci 1997; 17: 4325-4332.</ref>. | ||
Furthermore, Whiteside and Munglani have demonstrated that, following chronic nerve ligation injury, hyperalgesia develops in parallel with neuronal apoptosis. The administration of MK-801 prevents the former and significantly reduces the latter; from this, the authors suggest that apoptosis may contribute to the development and maintenance of hyperalgesia <ref>Whiteside GT, Munglani R. NMDAR antagonism prevents both the hyperalgesia and apoptosis induced by peripheral nerve injury. Pain 2001; 89: 287-294.</ref>. | Furthermore, Whiteside and Munglani have demonstrated that, following chronic nerve ligation injury, hyperalgesia develops in parallel with neuronal apoptosis. The administration of MK-801 prevents the former and significantly reduces the latter; from this, the authors suggest that apoptosis may contribute to the development and maintenance of hyperalgesia. <ref>Whiteside GT, Munglani R. NMDAR antagonism prevents both the hyperalgesia and apoptosis induced by peripheral nerve injury. Pain 2001; 89: 287-294.</ref><ref>https://www.geneticlifehacks.com/neurotransmitters/neurotransmitters-neurotransmitters/</ref> | ||
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