Excitatory synaptic transmission in the spinal substantia gelatinosa is under an inhibitory tone of endogenous adenosine

Excitatory synaptic transmission in the spinal substantia gelatinosa is under an inhibitory tone of endogenous adenosine
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DOI:
10.1016/j.neulet.2010.04.029
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发表时间:
2010-06
影响因子:
2.5
通讯作者:
L. Tian;G. Ji;Chen Wang;Xiaoguang Bai;Yan Lu;L. Xiong
L. Tian;G. Ji;Chen Wang;Xiaoguang Bai;Yan Lu;L. Xiong
中科院分区:
医学4区
文献类型:
--
作者:
L. Tian;G. Ji;Chen Wang;Xiaoguang Bai;Yan Lu;L. Xiong

文献摘要

相似文献

外源性腺苷在脊髓胶状质(SG)产生有效的突触抑制,该区域参与伤害性感受和温度感受机制。为探讨内源性腺苷对脊髓SG兴奋性突触传递的调节作用,对成年大鼠脊髓脑片SG神经元进行了全细胞电压钳记录。在所有对外源性腺苷敏感的SG神经元中,腺苷摄取抑制剂NBTI模拟腺苷对背根诱发EPSCs(EEPSCs)和小型自发性EPSCs(MEPSCs)的抑制作用。这些抑制作用可被腺苷A1受体拮抗剂DPCPX拮抗。在腺苷或腺苷A1受体激动剂(CHA、CCPA)抑制eEPSCs的情况下,DPCPX也能增强这些SG神经元中的eEPSCs。DPCPX经常在不改变mEPSC幅度的情况下增加mEPSC的频率,提示对腺苷A1受体的突触前作用。选择性A2(DMPX)和A2a(ZM 241385)腺苷受体拮抗剂对eEPSCs和mEPSCs均无或极小影响。腺苷降解酶,腺苷脱氨酶,模拟DPCPX对mEPSC频率的影响。我们的结论是,脊髓SG的兴奋性突触传递是通过激活A1受体而受到内源性腺苷抑制的。上述结果提示,脊髓SG内A1受体的背景活动可能与生理“伤害性阈值”的设定有关。
Exogenous adenosine produces potent synaptic inhibition in spinal substantia gelatinosa (SG), a region involved in nociceptive and thermoreceptive mechanisms. To examine the possibility that endogenous adenosine tonically modulates excitatory synaptic transmission in spinal SG, whole-cell, voltage-clamp recordings were made from SG neurons in adult rat spinal cord slices. In all SG neurons sensitive to exogenous adenosine, the adenosine uptake inhibitor, NBTI, mimics adenosine's inhibitory actions on dorsal root evoked EPSCs (eEPSCs) and miniature spontaneous EPSCs (mEPSCs). These inhibitory effects were antagonized by A1 adenosine receptor antagonist, DPCPX. DPCPX also potentates eEPSCs in those SG neurons in which adenosine or adenosine A1 receptor agonists (CHA, CCPA) suppressed eEPSCs. DPCPX often increases mEPSC frequency without altering mEPSC amplitude, suggesting presynaptic action on adenosine A1 receptors. Selective A2 (DMPX) and A2a (ZM 241385) adenosine receptor antagonists had no or minimal effects upon either eEPSCs or mEPSCs. The adenosine degrading enzyme, adenosine deaminase, mimicked the effects of DPCPX on the mEPSC frequency. We conclude that the excitatory synaptic transmission in the spinal SG is under an inhibitory tone of endogenous adenosine through the activation of A1 receptors. The present results suggested that the background activity of A1 receptors in the spinal SG might be contributed to setting the physiological “noceceptive thresholds”.