title: Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.
abstract: Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.
authors.affiliation: 1] Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan [2] Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.
authors.forename: Tatsunori
authors.initials: T
authors.lastname: Watanabe
authors.affiliation: Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.
authors.forename: Mika
authors.initials: M
authors.lastname: Sasaki
authors.affiliation: Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan.
authors.forename: Seiji
authors.initials: S
authors.lastname: Komagata
authors.affiliation: Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Tsukano
authors.affiliation: Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan.
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Hishida
authors.affiliation: Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Kohno
authors.affiliation: Department of Anesthesiology, School of Medicine, Niigata University, 1-757 Asahi-machi, Chuo-ku, Niigata 951-8510, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Baba
authors.affiliation: Department of Neurophysiology, Brain Research Institute, Niigata University,1-757 Asahi-machi, Chuo-ku, Niigata 951-8585, Japan.
authors.forename: Katsuei
authors.initials: K
authors.lastname: Shibuki
mesh_terms: D000818:Animals; D001643:Bridged Bicyclo Compounds / Q000494:pharmacology / Q000627:therapeutic use; D007511:Ischemia / Q000188:drug therapy / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000378:metabolism; D061848:Optical Imaging; D011312:Pressure; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists / Q000378:metabolism; D013003:Somatosensory Cortex / Q000187:drug effects / Q000503:physiopathology; D013116:Spinal Cord / Q000187:drug effects / Q000503:physiopathology*; D013848:Thigh / Q000098:blood supply
chemical_list: D001643:Bridged Bicyclo Compounds; D024101:Mitochondrial Proteins; D018094:Receptors, Metabotropic Glutamate; C104753:eglumetad