中国科学院心理研究所机构知识库

It has been widely accepted that the primary somatosensory cortex (SI) plays an essential role in the sensory-discriminative aspect of pain perception. However, it remains unclear whether the SI has a role in the descending modulation of pain. Although there are abundant fibers projecting back from sensory cortex to thalamic nuclei, and the influence of cortical modulation from SI on the thalamic nociceptive relay neurons has been addressed, little is known about how the cortical outputs modulate the nociceptive behaviors resulting from tissue injury or evoked by painful stimulation. The present study was designed to test whether the cortical outputs influenced the nociceptive behaviors using rat models of noxious thermal-induced acute pain, formalin-induced acute and CFA-evoked chronic inflammatory pain. The results showed that intracortical microinjection of GABA(A) agonist muscimol significantly reduced the first and second phase behaviors in formalin tests and elevated the nociceptive thresholds in the thermal stimulus-elicited acute pain, suggesting a facilitatory influence of SI on the acute pain sensation. By contrast, microinjection of GABA(A) antagonist bicuculline remarkably reduced the thermal hyperalgesia of the CFA-inflamed hindpaws, indicating an inhibitory effect of SI output in the chronic pain state. The opposite modulatory effects in acute and chronic pain states suggest that there exists a functional switch for the SI cortex at different stages of pain disease, which is of great significance for the biological adaptation.;It has been widely accepted that the primary somatosensory cortex (SI) plays an essential role in the sensory-discriminative aspect of pain perception. However, it remains unclear whether the SI has a role in the descending modulation of pain. Although there are abundant fibers projecting back from sensory cortex to thalamic nuclei, and the influence of cortical modulation from SI on the thalamic nociceptive relay neurons has been addressed, little is known about how the cortical outputs modulate the nociceptive behaviors resulting from tissue injury or evoked by painful stimulation. The present study was designed to test whether the cortical outputs influenced the nociceptive behaviors using rat models of noxious thermal-induced acute pain, formalin-induced acute and CFA-evoked chronic inflammatory pain. The results showed that intracortical microinjection of GABA(A) agonist muscimol significantly reduced the first and second phase behaviors in formalin tests and elevated the nociceptive thresholds in the thermal stimulus-elicited acute pain, suggesting a facilitatory influence of SI on the acute pain sensation. By contrast, microinjection of GABA(A) antagonist bicuculline remarkably reduced the thermal hyperalgesia of the CFA-inflamed hindpaws, indicating an inhibitory effect of SI output in the chronic pain state. The opposite modulatory effects in acute and chronic pain states suggest that there exists a functional switch for the SI cortex at different stages of pain disease, which is of great significance for the biological adaptation. (C) 2008 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.