大鼠大脑皮层体感Ⅱ区对中缝大核痛调制机能的调控及其与伏核为关系

我们以往的工作证明 SmⅡ是电针镇痛所需要的结构。本文进一步分析 SmⅡ参与电针镇痛的途径,看到损毁伏核(NAc)后,电针“足三里”激活 NRM,及抑制伤害性反应的效应明显减弱,甚至引起伤害性反应增大。表明 SmⅡ可能是通过边缘中脑系统的伏核对 NRM 进行调控,而参与痛调制功能。还指出对中枢某些结构有器质性损毁的病人行针刺治疗时应慎重,注意研究其实效。

The Control of Somatosensory Area Ⅱ of Cerebral Cortex on Nucles Raphe Magnus and Its Relation with Nucleus Accumbens

Our previous work have demonstrated that the stimulation of somatosensory area Ⅱ(Sm Ⅱ)of cerebral cortex or N.accumbens(NAc)could activate nucleus raphe magnus(NRM),produc-ing analgesia.The aim of this work is to study whether the effect of activation of Sm Ⅱ on neu-rons in NRM is related to NAc.The spontaneous discharges of NRM neurons and their nociceptive responses induced bystimulation of tail tip were recorded extracellularly with glass microelectrode.The effects ofstimulation of Sm Ⅱ on the NRM neurons were observed before and after lesion of NAc.Before lesion of NAc,the stimulation of Sm Ⅱ could activate NRM neurons,obviously in-creasing the firing rates in 0～10 minutes after stimulation(P<0.05～0.01),and their nocicep-tive responses were decreased in 0-10 and 20 minutes(P<0.01～0.001).After lesion of NAc,the firing rates having no clear change,and their nociceptive responses were even slightly en-hanced.It is suggested that the effect of activation of Sm Ⅱ on NRM neurons may need the relayvia the NAc.