Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons

Article Abstract:

The phenotypic switch of the A beta fibres in the myelinated primary sensory neurons leads to hypersensitivity to inflammatory pain. The A beta fibres change their phenotype to one resembling the pain fibres and express the substance P. This increases the synaptic transmission of neurons in the spinal cord and also magnifies the central response to painless stimuli. Inflammation leads to an increase in the A delta and C fibres peripheral terminal sensitivity. It also enhances the excitability of the spinal cord neurons.

Research, Allergy, Spinal cord, Nociceptors

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Overcoming inhibition

Article Abstract:

Partial recovery from complete injury to the spinal cord has been made possible by neutralizing a myelin-associated, neurite-growth inhibitor molecule. These molecules are present on oligodendrocytes and suppress axonal growth. Experiments have been conducted on rats and have not yet been tried on human beings. However, the findings are a major step towards the treatment of spinal cord injuries for which no successful remedies are available.

Care and treatment, Growth, Central nervous system, Axons, Regeneration (Biology), Spinal cord injuries

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Interleukin-1 beta-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity

Article Abstract:

Research is presented concerning the production of localized hypersensitivity to pain through the release of prostanoids following the induction of cyclooxygenase-2 as a result of inflamation.

Pain, Letter to the Editor, Prostanoids

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