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Inhibition of tonic spinal glutamatergic activity induces antinociception in the rat
Author(s) -
Tambeli Claudia H.,
Parada Carlos A.,
Levine Jon D.,
Gear Robert W.
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02204.x
Subject(s) - kainate receptor , nociception , glutamatergic , ampa receptor , neuroscience , tonic (physiology) , chemistry , cnqx , pharmacology , nmda receptor , spinal cord , glutamate receptor , receptor , medicine , biology , biochemistry
Summary Inhibition of tonic activity in spino‐supraspinal projection neurons induces heterosegmental antinociception that is mediated by opioid receptors in nucleus accumbens. To investigate the origin of this tonic activity, we evaluated the ability of inhibiting neurotransmission in the spinal cord to produce heterosegmental antinociception in the trigeminal nociceptive jaw‐opening reflex (JOR) in the rat. Spinal intrathecal administration of calcium channel blockers attenuated the JOR, suggesting that the tonic spinal activity depends on synaptic input. To identify the excitatory neurotransmitter receptors involved, selective antagonists for AMPA/kainate, mGluR 1 , NMDA or NK 1 receptors were administered intrathecally to the spinal cord. The AMPA/kainate and mGluR 1 receptor antagonists, but not the NMDA or NK 1 receptor antagonists, induced antinociception, which was antagonized by intra‐accumbens administration of the selective µ‐opioid receptor antagonist CTOP. Thus, inhibition of tonic spinal glutamatergic activity resulted in supraspinally mediated antinociception. As this antinociception occurred in the absence of interventions that would produce a facilitated nociceptive state, this tonic glutamatergic activity is important in setting nociceptive threshold.