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首页> 外文期刊>Neurophysiology >Modulation of Synaptic Reactions of the 'Nociceptive' Neurons in the Cat Cortex upon Stimulation of the Periaqueductal Gray and Application of Some Pharmacological Agents
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Modulation of Synaptic Reactions of the 'Nociceptive' Neurons in the Cat Cortex upon Stimulation of the Periaqueductal Gray and Application of Some Pharmacological Agents

机译:在刺激刺激猫皮层中“伤害性”神经元的突触反应在刺激面纱灰色的灰色和应用中的应用

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We examined the effects of electrical stimulation of the periaqueductal gray (PAG) and systemic morphine injections on postsynaptic processes in neurons of the cat somatosensory cortex, which were activated by nociceptive influences. Stimulation of the PAG resulted in long-lasting suppression of synaptic reactions induced by stimulation of dental pulp nociceptors. There was certain parallelism within the conditioning effects of PAG stimulation and effects of systemic introduction of morphine. Ionophoretic application of strychnine on such pyramidal cortical neurons did not evoke paroxysmal depolarization shifts (PDSh) of the membrane potential in such neurons. At the same time, surface application of this agent on the cortex (which influenced extensive populations of cortical neurons) resulted in the development of considerable PDShs. This observation confirms the synaptic nature of the above shifts. Applications of strychnine using both techniques resulted in the blockade of, first of all, early IPSP components in pyramidal neurons but did not affect significantly late components of these potentials; this is indicative of different geneses of the above components. It is supposed that the early IPSP component is generated due to activation of axo-somatic inhibitory synapses, while the late component of such reactions is related to activation of inhibitory synapses localized in the dendrites. The mechanisms of modulation of postsynaptic reactions of somatosensory cortex neurons developing upon activation of high-threshold (nociceptive) afferent inputs are discussed. Such modulation is probably based on changes in both pre- and post-synaptic intracortical cell structures.
机译:我们研究了胰刺激的电气刺激和全身性吗啡注射对猫生长源性皮质的神经元突触后过程的影响,这些过程被伤害的影响激活。刺激PAG导致通过刺激牙髓伤害患者诱导的突触反应的长期抑制。 PAG刺激的调理效果存在一定的平行性,并对吗啡引入的影响。在这种锥体皮质神经元对这种锥形皮质神经元的滴水酮的热应用并未引起这种神经元膜电位的阵发性去极化移位(PDSH)。与此同时,该试剂对皮质的表面施加(影响皮质神经元的广泛群体)导致了相当大的PDSH。该观察结果证实了上述班次的突触性质。使用这两种技术的斯特妥尼的应用导致封锁,首先是金字塔神经元的早期IPSP组件,但不影响这些潜力的显着晚期部件;这表明上述组分的不同基因。假设早期的IPSP组分是由于轴身抑制突起的激活而产生的,而这种反应的后期组分与树突中局部化的抑制突触的激活有关。讨论了在激活高阈值(Noceicptive)传入输入时发育的躯体感染型皮质神经元的后突触后反应的机制。这种调制可能基于突触前和后突触后的地形细胞结构的变化。

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