Systematic administration of B vitamins attenuates neuropathic hyperalgesia and reduces spinal neuron injury following temporary spinal cord ischaemia in rats

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Abstract
Background: B vitamins have been demonstrated to be effective in treating chronic pain due to peripheral nerve injury. We investigated whether B vitamins could alleviate neuropathic pain and reduce neuron injury following temporary ischaemia in a rat model of spinal cord ischaemia‐reperfusion injury (SCII).Methods: SCII was produced by transiently blocking the unilateral lumbar arteries in adult male Sprague‐Dawley rats. Behavioural and neurochemical signs of neuropathic pain and spinal neuron injury were analysed with and without B vitamin treatment.Results: SCII caused behavioural thermal hyperalgesia and mechanical allodynia and neurochemical alterations, including increased expression of the vanilloid receptor 1 (VR1) and induction of c‐Fos, as well as activation of the astrocytes and microglial cells in the spinal cord. Repetitive systemic administration of vitamin B complex (B1/B6/B12 at 33/33/0.5 mg/kg, i.p., daily, for 7–14 consecutive days) significantly reduced thermal hyperalgesia and the increased expression of VR1 and c‐Fos, as well as activation of the astrocytes and microglial cells. SCII caused a dramatic decrease of the expression of the rate‐limiting enzyme glutamic acid decarboxylase‐65 (GAD65), which synthesizes γ‐aminobutyric acid (GABA) in the axonal terminals, and β‐III‐tubulin, and also caused loss of Nissl bodies in the spinal cord. These alterations were largely prevented and rescued by the B vitamin treatment.Conclusions: These findings support the idea that the B vitamins are capable of neuroprotection and antinociception during spinal cord injury due to temporary ischaemia. Rescuing the loss of inhibitory GABAergic tone may reduce spinal central sensitization and contribute to B vitamin‐induced analgesia.

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