STIMULATION-PRODUCED DESCENDING INHIBITION FROM THE PERIAQUEDUCTAL GRAY AND NUCLEUS RAPHE MAGNUS IN THE RAT - MEDIATION BY SPINAL MONOAMINES BUT NOT OPIOIDS
STIMULATION-PRODUCED DESCENDING INHIBITION FROM THE PERIAQUEDUCTAL GRAY AND NUCLEUS RAPHE MAGNUS IN THE RAT - MEDIATION BY SPINAL MONOAMINES BUT NOT OPIOIDS
复制标题
DOI：
10.1016/0304-3959(87)90012-1
复制
发表时间：
1987-10-01
期刊：
影响因子：
7.4
通讯作者：
GEBHART, GF
中科院分区：
文献类型：
--
作者：
AIMONE, LD;JONES, SL;GEBHART, GF
中脑导水管周围灰质（PAG）或中缝大髓核（NRM）的局灶性电刺激抑制脊髓伤害性信息传递和伤害性反射。本研究的目的是在轻度戊巴比妥麻醉的大鼠中，评价在PAG或NRM中介导的脊髓神经递质。为了表征介导TF反射抑制的神经递质，将选择性药理学拮抗剂给予腰椎鞘内空间。建立PAG或NRM中抑制TF反射的刺激阈值，并测定鞘内施用酚妥拉明、育亨宾、哌唑嗪、麦角新碱（最初15 μ g，累积30 μ g）或纳洛酮（最初10 μ g，累积20 μ g）对TF抑制阈值的影响。酚妥拉明、育亨宾和麦角新碱增加PAG和NRM的刺激强度，抑制TF反射;哌唑嗪和纳洛酮没有效果。通过局灶性电刺激在PAG或NRM中产生的下降抑制部分由脊髓血清素能和/或α 2-肾上腺素能受体介导。纳洛酮鞘内和静脉内给药;然而，没有发现阿片受体在中脑或髓质下行抑制中的作用。
Focal electrical stimulation in the midbrain periaqueductal gray (PAG) or medullary nucleus raphe magnus (NRM) inhibits spinal nociceptive transmission and nociceptive reflexes. The purpose of this study was to evaluate, in lightly pentobarbital-anesthetized rats, the spinal neurotransmitter(s) mediating in the PAG or NRM. To characterize the neurotransmitter(s) mediating inhibition of the TF reflex, selective pharmacologic antagonists were administered into the lumbar intrathecal space. Stimulation thresholds in the PAG or NRM for inhibition of the TF reflex were established and the effects of intrathecally administered phentolamine, yohimbine, prazosin, methysergide (15 .mu.g initially, 30 .mu.g cumulative) or naloxone (10 .mu.g initially, 20 .mu.g cumulative) on TF inhibitory thresholds determined. Phentolamine, yohimbine and methysergide increased the intensity of stimulation in the PAG and the NRM for inhibition of the TF reflex; prazosin and naloxone had no effect. Descending inhibition produced by focal electrical stimulation in the PAG or NRM is mediated in part by spinal serotonergic and/or .alpha.2-adrenergic receptors. Naloxone was administered both intrathecally and intravenously; however, a role for opioid receptors in descending inhibition from the midbrain or medulla was not found.