The activation of nicotinic acetylcholine receptors enhances the inhibitory synaptic transmission in the deep dorsal horn neurons of the adult rat spinal cord
The activation of nicotinic acetylcholine receptors enhances the inhibitory synaptic transmission in the deep dorsal horn neurons of the adult rat spinal cord
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DOI：
10.1186/1744-8069-3-26
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发表时间：
2007-09-25
期刊：
影响因子：
3.3
通讯作者：
Yoshida, Munehito
中科院分区：
文献类型：
--
作者：
Takeda, Daisuke;Nakatsuka, Terumasa;Yoshida, Munehito
脊髓背角浅层的烟碱型乙酰胆碱受体（nAChRs）可以调节躯体感觉信息。尽管如此，nAChRs在成年动物深背角中的功能意义仍不清楚。使用全细胞膜片钳记录在成年大鼠脊髓V层神经元，我们调查是否激活的nAChRs可以调节抑制性突触传递在深背角。在CNQX和APV的存在下，阻断兴奋性突触能传递，浴应用尼古丁（100 μ M）显着增加了自发抑制性突触后电流（sIPSC）的频率在几乎所有的神经元测试。尼古丁的作用被N-甲基-4-（3-吡啶基）-3-丁烯-1-胺（RJR-2403，100 μ M）（一种α 4 β 2-nAChR激动剂）模拟，也被胆碱（10 mM）（一种α 7- nAChR激动剂）模拟。尼古丁的作用被nAChR拮抗剂美加明（5 μ M）完全阻断。在河豚毒素（0.5 μ M）的存在下，尼古丁（100 μ M）显着增加了微型IPSC频率。另一方面，RJR- 2403（100 μ M）或胆碱（10 mM）不影响微型IPSC。当细胞保持在-60 mV时，尼古丁（100 μ M）的应用也在所有测试的V层神经元中诱发了大的内向电流。同样，RJR- 2403（100 μ M）诱导的内向电流在大多数的V层神经元检查。另一方面，胆碱（10 mM）没有引起任何可检测的全细胞电流。这些结果表明，几个nAChR亚型表达的突触前终端，preterminals，和神经元细胞体在椎板V，这些nAChR参与调制的抑制性突触活动在脊髓深背角。
Somatosensory information can be modulated by nicotinic acetylcholine receptors (nAChRs) in the superficial dorsal horn of the spinal cord. Nonetheless, the functional significance of nAChRs in the deep dorsal horn of adult animals remains unclear. Using whole-cell patch-clamp recordings from lamina V neurons in the adult rat spinal cord, we investigated whether the activation of nAChRs could modulate the inhibitory synaptic transmission in the deep dorsal horn. In the presence of CNQX and APV to block excitatory glutamatergic synaptic transmission, bath applications of nicotine ( 100 mu M) significantly increased the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in almost all neurons tested. The effect of nicotine was mimicked by N-methyl-4-( 3-pyridinyl)-3-butene-1-amine (RJR-2403, 100 mu M), an alpha 4 beta 2-nAChR agonist, and was also mimicked by choline ( 10 mM), an alpha 7- nAChR agonist. The effect of nicotine was completely blocked by the nAChR antagonist mecamylamine ( 5 mu M). In the presence of tetrodotoxin ( 0.5 mu M), nicotine ( 100 mu M) significantly increased the miniature IPSC frequency. On the other hand, RJR- 2403 ( 100 mu M) or choline ( 10 mM) did not affect miniature IPSCs. The application of nicotine ( 100 mu M) also evoked a large inward current in all lamina V neurons tested when cells were held at -60 mV. Similarly, RJR- 2403 ( 100 mu M) induced inward currents in the majority of lamina V neurons examined. On the other hand, choline ( 10 mM) did not elicit any detectable whole-cell currents. These results suggest that several nAChR subtypes are expressed on the presynaptic terminals, preterminals, and neuronal cell bodies within lamina V and that these nAChRs are involved in the modulation of inhibitory synaptic activity in the deep dorsal horn of the spinal cord.