2009
DOI: 10.1007/s00540-009-0767-y
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Suppression of the descending inhibitory pathway by continuous thoracic intrathecal lidocaine infusion reduces the thermal threshold of the tail-flick response in rats

Abstract: Continuous thoracic blockade by local anesthetic resulted in reversible suppression of descending inhibitory pathways for varying durations. Such blockade may provide further information regarding nociceptive transmission and the mechanisms of antinociception in animals.

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Cited by 2 publications
(2 citation statements)
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“… 2 Unlike neural circuits in the brain, spinal dorsal neurons, which are second‐order neurons in the process of nociception, receive dominated glutamate from primary afferent fibers and the descending inhibitory pathway from the higher brain regions, contributed to mediating and influencing nociceptive transmission. 3 Nerve injury including rodent model of SNL may generate maladaptive dorsal horn plasticity and lead to pain states associated with alterations in N‐methyl‐D‐aspartate (NMDA) receptor‐mediated hypersensitivity, disinhibition of descending γ‐aminobutyric acid (GABAergic) /glycinergic inhibitory neurotransmission, and activation of glial cells, especially microglia. 2 , 4 , 5 , 6 The coordinative activity of microglia and neurons in brain diseases has been intensively studied, 7 , 8 , 9 while microglial‐derived factors sensitize sensory processing through tumor necrosis factor (TNF)‐α, IL‐6, IL‐1β, and P2X inotropic receptors and leading to restore spinally mediated nocifensive reflexes mediated proinflammatory cytokines.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“… 2 Unlike neural circuits in the brain, spinal dorsal neurons, which are second‐order neurons in the process of nociception, receive dominated glutamate from primary afferent fibers and the descending inhibitory pathway from the higher brain regions, contributed to mediating and influencing nociceptive transmission. 3 Nerve injury including rodent model of SNL may generate maladaptive dorsal horn plasticity and lead to pain states associated with alterations in N‐methyl‐D‐aspartate (NMDA) receptor‐mediated hypersensitivity, disinhibition of descending γ‐aminobutyric acid (GABAergic) /glycinergic inhibitory neurotransmission, and activation of glial cells, especially microglia. 2 , 4 , 5 , 6 The coordinative activity of microglia and neurons in brain diseases has been intensively studied, 7 , 8 , 9 while microglial‐derived factors sensitize sensory processing through tumor necrosis factor (TNF)‐α, IL‐6, IL‐1β, and P2X inotropic receptors and leading to restore spinally mediated nocifensive reflexes mediated proinflammatory cytokines.…”
Section: Introductionmentioning
confidence: 99%
“…The unique axonal branches of the dorsal root ganglia could easily detect and immediately respond to injurious stimuli by transmitting information from the periphery to the brain through the spinal cord 2 . Unlike neural circuits in the brain, spinal dorsal neurons, which are second‐order neurons in the process of nociception, receive dominated glutamate from primary afferent fibers and the descending inhibitory pathway from the higher brain regions, contributed to mediating and influencing nociceptive transmission 3 2,4–6 …”
Section: Introductionmentioning
confidence: 99%