内吗啡肽-1对成年大鼠脊髓胶状质内突触传递的抑制作用强于内吗啡肽-2(英文)

本实验采用全细胞电压钳记录方法,研究了内吗啡肽1(EM1)和内吗啡肽2(EM2)对脊髓背角胶状质神经元突触传递的抑制性作用。EM1(1μmol/L)和EM2(1μmol/L)都能够显著抑制微小兴奋性突触后电流(mEPSCs)和微小抑制性突触后电流(mIPSCs)的频率而不改变其幅值。这种抑制作用能被μ受体选择性拮抗剂βfunaltrexamine(βFNA,10μmol/L)阻断。值得注意的是,EM1对mEPSCs和mIPSCs的频率的抑制作用强于EM2。上述结果提示在脊髓胶状质,内吗啡肽通过激活突触前膜上的μ受体,抑制兴奋性和抑制性的突触传递;与EM2相比,EM1可能是脊髓水平的更强效的内源性镇痛剂。

ENDOMORPHIN-1 IS MORE POTENT THAN ENDOMORPHIN-2 IN INHIBITION OF SYNAPTIC TRANSMISSION IN SUBSTANTIA GELATINOSA OF ADULT RAT SPINAL CORD

Effects of endomorphin-1 (EM-1) and endomorphin-2 (EM-2) on synaptic transmission were investigated on neurons in substantia gelatinosa (SG) of the spinal dorsal horn by whole-cell voltage clamp recording. Both EM-1 (1 μmol/L) and EM-2 (1 μmol/L)remarkably reduced the frequency but not the amplitude of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs). These effects were antagonized by 3-funaltrexamine ( β-FNA, 10 μmol/L), a selective μ-opioid receptor antagonist. Noticeably, EM-1 showed higher potency in decreasing the frequency of mEPSCs and mIPSCs than that of EM-2. These results indicate that EMs suppress both excitatory and inhibitory synaptic transmission by activating presynaptic μ-opioid receptors in the SG and EM-1, compared with EM-2, might be a more potent endogenous analgesic at the spinal cord level.