Papers

Peer-reviewed
Jul, 2015

Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice

SCIENTIFIC REPORTS
  • Tatsunori Watanabe
  • ,
  • Mika Sasaki
  • ,
  • Seiji Komagata
  • ,
  • Hiroaki Tsukano
  • ,
  • Ryuichi Hishida
  • ,
  • Tatsuro Kohno
  • ,
  • Hiroshi Baba
  • ,
  • Katsuei Shibuki

Volume
5
Number
First page
11191
Last page
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1038/srep11191
Publisher
NATURE PUBLISHING GROUP

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 (S-1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S-1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S-1 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.

Link information
DOI
https://doi.org/10.1038/srep11191
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26165560
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000357798000001&DestApp=WOS_CPL
ID information
  • DOI : 10.1038/srep11191
  • ISSN : 2045-2322
  • Pubmed ID : 26165560
  • Web of Science ID : WOS:000357798000001

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