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首页> 外文期刊>Molecular pain >Changes in synaptic transmission of substantia gelatinosa neurons after spinal cord hemisection revealed by analysis using in?vivo patch-clamp recording
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Changes in synaptic transmission of substantia gelatinosa neurons after spinal cord hemisection revealed by analysis using in?vivo patch-clamp recording

机译:使用体内膜片钳记录分析揭示脊髓半切后明胶质神经元突触传递的变化

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摘要

After spinal cord injury, central neuropathic pain develops in the majority of spinal cord injury patients. Spinal hemisection in rats, which has been developed as an animal model of spinal cord injury in humans, results in hyperexcitation of spinal dorsal horn neurons soon after the hemisection and thereafter. The hyperexcitation is likely caused by permanent elimination of the descending pain systems. We examined the change in synaptic transmission of substantia gelatinosa neurons following acute spinal hemisection by using an in?vivo whole-cell patch-clamp technique. An increased spontaneous action potential firings of substantia gelatinosa neurons was detected in hemisected rats compared with that in control animals. The frequencies and amplitudes of spontaneous excitatory postsynaptic currents and of evoked excitatory postsynaptic currentss in response to non-noxious and noxious stimuli were not different between hemisected and control animals. On the contrary, the amplitude and frequency of spontaneous inhibitory postsynaptic currents of substantia gelatinosa neurons in hemisected animals were significantly smaller and lower, respectively, than those in control animals (P?multi-receptive substantia gelatinosa neurons, which exhibit action potential firing in response to non-noxious and noxious stimuli, was much larger in hemisected animals than in control animals. These suggest that substantia gelatinosa neurons receive tonic inhibition by spinal inhibitory interneurons which generate persistent action potentials. Spinal hemisection results in hyperexcitation of substantia gelatinosa neurons at least in part by eliminating the tonic descending control of spinal inhibitory interneurons from supraspinal levels.
机译:脊髓损伤后,大多数脊髓损伤患者会出现中枢神经性疼痛。大鼠的脊髓半切已被开发为人类脊髓损伤的动物模型,导致半切后及之后的脊髓背角神经元过度兴奋。过度兴奋可能是由于永久消除了下行疼痛系统而引起的。我们通过使用体内全细胞膜片钳技术检查了急性脊髓半切后明胶质神经元突触传递的变化。与对照动物相比,在半切的大鼠中发现了明胶质神经元的自发动作电位放电。在半切除和对照动物之间,对非有害和有害刺激的自发性兴奋性突触后电流和诱发的兴奋性突触后电流的频率和幅度没有差异。相反,半体切除的动物中明胶质神经元的自发抑制性突触后电流的幅度和频率分别比对照动物(P?多接受明胶性神经质神经元,它们在响应中表现出动作电位)显着更小和更低。偏侧动物对非有害和有害刺激的影响要比对照动物大得多,这表明明胶质神经元受到脊髓抑制性中间神经元的强直抑制,产生持续的动作电位,脊髓半切至少导致明胶质神经元过度兴奋。通过消除脊柱上水平对脊柱抑制性中间神经元的强直下降控制来实现这一目标。

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