PAIN
Volume 143, Issue 3 , Pages 228-232, June 2009

Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord

  • Claudia H. Tambeli

      Affiliations

    • Department of Oral and Maxillofacial Surgery, NIH Pain Center (UCSF), University of California at San Francisco, Rm C-522, Box 0440, San Francisco, CA 94143-0440, USA
    • Faculty of Dentistry of Piracicaba, University of Campinas, Brazil
    • ,
  • Jon D. Levine

      Affiliations

    • Department of Oral and Maxillofacial Surgery, NIH Pain Center (UCSF), University of California at San Francisco, Rm C-522, Box 0440, San Francisco, CA 94143-0440, USA
    • Department of Medicine, University of California, San Francisco, USA
    • ,
  • Robert W. Gear

      Affiliations

    • Department of Oral and Maxillofacial Surgery, NIH Pain Center (UCSF), University of California at San Francisco, Rm C-522, Box 0440, San Francisco, CA 94143-0440, USA
    • Corresponding Author InformationCorresponding author. Tel.: +1 415 476 4902; fax: +1 415 476 6305.

Received 21 November 2008; received in revised form 3 February 2009; accepted 5 March 2009. published online 17 April 2009.

Abstract 

The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors.

Keywords: Pain-induced analgesia, Nucleus accumbens, Spinal cord, Rat, Antinociception, Capsaicin

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PII: S0304-3959(09)00154-7

doi:10.1016/j.pain.2009.03.005

PAIN
Volume 143, Issue 3 , Pages 228-232, June 2009

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