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

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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yu, C-Z Liu, Y-P Liu, S. Yan, M. Hu, S-J Song, X-J
Description	Country affiliation: China Author Affiliation: Yu CZ ( Institute of Neurosciences, The Fourth Military Medical University, Xi'an, China.)
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 Î³-aminobutyric acid (GABA) in the axonal terminals, and ß-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.
File Format	HTM / HTML
ISSN	10903801
Issue Number	1
Volume Number	18
e-ISSN	15322149
Journal	European Journal of Pain
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2014-01-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neurology Discipline Anesthesiology Hyperalgesia Drug Therapy Neuralgia Neurons Drug Effects Spinal Cord Ischemia Complications Vitamin B Complex Therapeutic Use Animals Blotting, Western Glutamate Decarboxylase Metabolism Hot Temperature Etiology Immunohistochemistry Male Motor Activity Pathology Nissl Bodies Physical Stimulation Proto-oncogene Proteins C-fos Biosynthesis Rats Rats, Sprague-dawley Reperfusion Injury Tubulin Administration & Dosage Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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