title: Systematic administration of B vitamins attenuates neuropathic hyperalgesia and reduces spinal neuron injury following temporary spinal cord ischaemia in rats.
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.
authors.affiliation: Institute of Neurosciences, The Fourth Military Medical University, Xi'an, China.
authors.forename: C-Z
authors.initials: CZ
authors.lastname: Yu
authors.forename: Y-P
authors.initials: YP
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Liu
authors.forename: M
authors.initials: M
authors.lastname: Yan
authors.forename: S-J
authors.initials: SJ
authors.lastname: Hu
authors.forename: X-J
authors.initials: XJ
authors.lastname: Song
mesh_terms: D000818:Animals; D015153:Blotting, Western; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006358:Hot Temperature; D006930:Hyperalgesia / Q000188:drug therapy* / Q000209:etiology; D007150:Immunohistochemistry; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D009437:Neuralgia / Q000188:drug therapy* / Q000209:etiology; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D009562:Nissl Bodies / Q000187:drug effects; D010812:Physical Stimulation; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy / Q000473:pathology; D020760:Spinal Cord Ischemia / Q000150:complications* / Q000473:pathology; D014404:Tubulin / Q000096:biosynthesis; D014803:Vitamin B Complex / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D014404:Tubulin; D014803:Vitamin B Complex; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2