辣椒素受体参与骶髓后联合核神经元突触传递

目的研究辣椒素受体对大鼠骶髓后联合核(SDCN)神经元突触传递的影响。方法在脊髓骶段横切薄片上,利用全细胞膜片钳法记录骶髓后联合核神经元谷氨酸能兴奋性突触后电流(EPSCs)和γ-氨基丁酸(GABA)能抑制性突触后电流(IPSCs),比较激动辣椒素受体后上述突触电流的变化;观察激动辣椒素受体对SDCN神经元动作电位发放的影响。结果辣椒素受体被其特异性激动剂辣椒素(1μmol.L-1)激动后,自发EPSCs(sEPSCs)的频率和振幅均有明显增加(P<0.05,n=17)。在河豚毒素(0.5μmol.L-1)存在的条件下,辣椒素明显增加微小EPSCs(mEPSCs)的频率(P<0.01,n=13),但对mEPSCs的振幅无影响(P>0.05,n=13),提示辣椒素的作用在突触前。辣椒素也明显增加动作电位发放(P<0.05,n=19)。上述作用均可被辣椒素受体特异性拮抗剂capsazepine(10μmol.L-1)阻断。辣椒素也增加GABA能的自发IPSCs(sIPSCs)的频率(P<0.05,n=20),但对其不依赖动作电位的微小IPSCs(mIPSCs)的频率或振幅均无作用(P>0.05,n=9)。结论在SDCN,辣椒素受体主要表达于兴奋性突触终末;激动辣椒素受体影响兴奋性和抑制性突触活动,并可能参与痛觉信息在脊髓水平的传递和调制。

Involvement of capsaicin receptors in synaptic transmission in sacral dorsal commissural nucleus neurons

Aim To investigate the role of capsaicin receptors in synaptic transmission in sacral dorsal commissural nucleus(SDCN) neurons of rat spinal cord.Methods Whole-cell voltage-clamp recordings on spinal cord slice were used to investigate glutamate-mediated excitatory postsynaptic currents(EPSCs) and γ-aminobutyric acid(GABA)-mediated inhibitory postsynaptic currents(IPSCs);capsaicin effect on action potentials discharge was also accessed.Results Activation of capsaicin receptors by a specific agonist,capsaicin(1 μmol·L-1),significantly enhanced both frequency and amplitude of spontaneous EPSCs(sEPSCs)(P<0.05,n=17).In the presence of tedrodotoxin(TTX),capsaicin increased miniature EPSCs(mEPSCs) frequency(P<0.01,n=13) but not amplitude distribution(P>0.05,n=13),indicating a presynaptic action.Capsaicin also significantly accelerated action potential discharge(P<0.01,n=19).Capsaicin action was abolished by pretreatment of a specific antagonist,capsazepine.Capsaicin also enhanced spontaneous IPSCs(sIPSCs) frequency(P<0.05,n=20),but had no effect on either frequency or amplitude of miniature IPSCs(mIPSCs)(P>0.05,n=9).Conclusion Capsaicin receptors are exclusively expressed at presynaptic terminals of excitatory glutamatergic terminals to SDCN neurons;activation of capsaicin receptors modulates excitatory and inhibitory synaptic transmission in SDCN which may contribute to nociceptive information transmission and modulation at spinal cord level.