Modulation by adenosine of aδ and c primary-afferent glutamatergic transmission in adult rat substantia gelatinosa neurons
Modulation by adenosine of aδ and c primary-afferent glutamatergic transmission in adult rat substantia gelatinosa neurons
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DOI：
10.1016/j.neuroscience.2004.01.029
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发表时间：
2004-12
期刊：
影响因子：
3.3
通讯作者：
L. Lao;Y. Kawasaki;K. Yang;T. Fujita;E. Kumamoto
中科院分区：
文献类型：
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作者：
L. Lao;Y. Kawasaki;K. Yang;T. Fujita;E. Kumamoto
本研究观察了腺苷对成年大鼠脊髓薄片胶状质（SG）神经元单突触Aδ和C初级传入兴奋性突触后电流（EPSC）的作用。在67%的被检神经元中，腺苷可逆地降低A δ纤维EPSC的振幅，而在13%的被检神经元中，A δ纤维EPSC的振幅被降低或不受影响，在腺苷洗脱后，A δ纤维EPSC的振幅持续增加数分钟。其余的神经元没有表现出幅度的变化。腺苷对Aδ纤维EPSC振幅的降低呈剂量依赖性，半数抑制有效浓度（EC 50）值为217 μM。在配对脉冲刺激下，腺苷的第二与第一Aδ纤维EPSC振幅之比大于对照组的EPSC振幅之比，提示腺苷的突触前作用。在69%的受试神经元中，腺苷（100 μM）可逆地降低C纤维EPSC的幅度，其程度与Aδ纤维EPSC相当;其余神经元没有腺苷作用。腺苷在Aδ纤维和C纤维EPSC均被激发的神经元中也有类似的抑制作用。A1受体激动剂N6-环戊基腺苷（1 μM）可诱导Aδ纤维或C纤维EPSC振幅的类似降低，而A1受体拮抗剂8-环戊基-1，3-二丙基黄嘌呤（1 μM）的存在下未观察到腺苷诱导的降低。A2 a激动剂CGS 21680（1 μM）对Aδ纤维EPSC振幅无显著影响。它的结论是，腺苷突触前抑制单突触Aδ-纤维和C-纤维的传输，通过激活A1受体在许多但不是所有的SG神经元相似的程度，这可能有助于至少一部分的抗伤害性通过鞘内注射给药腺苷类似物，可能是内源性腺苷。
The present study examined the actions of adenosine on monosynaptic Aδ and C primary-afferent excitatory postsynaptic currents (EPSCs) recorded from substantia gelatinosa (SG) neurons of an adult rat spinal cord slice. In 67% of the neurons examined, adenosine reversibly decreased the amplitude of the Aδ-fiber EPSC, while in 13% of the neurons the amplitude was reduced or unaffected, which was followed by its increase persisting for several minutes after adenosine washout. The remaining neurons did not exhibit a change in the amplitude. The reduction in Aδ-fiber EPSC amplitude by adenosine was dose-dependent with an effective concentration for half-inhibition (EC50) value of 217 μM. When examined by using a paired-pulse stimulus, a ratio of the second to first Aδ-fiber EPSC amplitude under the reduction was larger than that of EPSC amplitude in the control, suggesting a presynaptic action of adenosine. In 69% of the neurons tested, the C-fiber EPSC was reversibly decreased in amplitude by adenosine (100 μM) by an extent comparable to that of Aδ-fiber EPSC; the remaining neurons were without adenosine actions. Similar inhibitory actions of adenosine were also seen in neurons where both Aδ-fiber and C-fiber EPSCs were elicited. Similar reduction in the Aδ-fiber or C-fiber EPSC amplitude was induced by an A1adenosine-receptor agonist, N6-cyclopentyladenosine (1 μM), and the adenosine-induced reduction was not observed in the presence of an A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (1 μM). An A2aagonist, CGS 21680 (1 μM), did not significantly affect the Aδ-fiber EPSC amplitude. It is concluded that adenosine presynaptically inhibits monosynaptic Aδ-fiber and C-fiber transmission by a similar extent through the activation of the A1receptor in many but not all SG neurons; this could contribute to at least a part of antinociception by intrathecally administered adenosine analogues and probably by endogenous adenosine.