Gebhart G F, Ossipov M H
J Neurosci. 1986 Mar;6(3):701-13. doi: 10.1523/JNEUROSCI.06-03-00701.1986.
Inhibition of the spinal nociceptive tail-flick (TF) reflex by focal electrical stimulation in the caudal medulla was examined and characterized in lightly pentobarbital-anesthetized rats. Systematic mapping studies revealed that inhibition of the TF reflex was produced at low intensities of stimulation (12.5-25 microA) only from the lateral reticular nucleus (LRN). Areas dorsal and medial to the LRN required higher intensities of stimulation to produce descending inhibition of the TF reflex, likely reflecting spread of current to the LRN at these higher intensities of stimulation (50-100 microA). At threshold inhibitory intensities of stimulation in the LRN, changes in blood pressure were not produced. Strength-duration characterization of stimulation and the microinjection of glutamate into the LRN at the same site where focal electrical stimulation was effective suggest that the descending inhibition produced arises from activation of cell bodies in the LRN. The intrathecal administration of a variety of pharmacological antagonists revealed the descending inhibition produced by stimulation in the LRN to be mediated at least in part by spinal alpha 2-adrenoceptors. These findings, together with previous observations, suggest a role for the LRN in the centrifugal modulation of spinal nociceptive transmission.
在轻度戊巴比妥麻醉的大鼠中,研究并表征了延髓尾部局灶性电刺激对脊髓伤害性甩尾(TF)反射的抑制作用。系统的图谱研究表明,仅在低强度刺激(12.5 - 25微安)下,外侧网状核(LRN)才能产生对TF反射的抑制。LRN背侧和内侧区域需要更高强度的刺激才能产生对TF反射的下行抑制,这可能反映了在这些更高强度刺激(50 - 100微安)下电流扩散到了LRN。在LRN中产生阈值抑制性刺激时,未引起血压变化。刺激的强度 - 持续时间特性以及在局灶性电刺激有效的同一部位向LRN微量注射谷氨酸表明,产生的下行抑制源于LRN中细胞体的激活。鞘内注射多种药理拮抗剂表明,LRN刺激产生的下行抑制至少部分由脊髓α₂ - 肾上腺素能受体介导。这些发现与先前的观察结果一起,提示了LRN在脊髓伤害性传递的离心调节中的作用。