Electrophysiological responses of neurons in the rat spinal cord to nitric oxide
Electrophysiological responses of neurons in the rat spinal cord to nitric oxide
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DOI：
10.1016/s0306-4522(96)00495-2
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发表时间：
1997-03-01
期刊：
影响因子：
3.3
通讯作者：
Schmid, HA
中科院分区：
文献类型：
--
作者：
Pehl, U;Schmid, HA
利用细胞外记录技术研究了含一氧化氮溶液和不同一氧化氮供体对大鼠脊髓切片中一氧化氮合酶高表达区自发活动神经元的影响。在X层中，93%的神经元（n=84）在一氧化氮供体硝普钠的灌注下增加了放电速率，2%的神经元降低了放电速率。相比之下，49%的I和II层神经元（n=90）被抑制，只有28%的神经元被激活。这两种效应都是由于硝普钠的突触后作用，因为它们仍然可以在含有0.3 mM Ca2+和9 mM Mg2+的介质中观察到，已知阻断突触传递。8-溴环- gmp的应用对硝普钠激发的神经元均有兴奋作用，对硝普钠抑制的细胞均有抑制作用（n=25）。这种作用与s -溴环amp的作用不同，s -溴环amp只模拟硝普钠的兴奋反应，而没有抑制反应。这些结果提供了脊髓一氧化氮可以直接引起脊髓神经元电活动的兴奋或抑制的证据。从我们的结果中得出的另一个更普遍的结论是，一氧化氮诱导的环gmp的产生本身并不能预测对神经元活动的兴奋或抑制作用，这必须单独确定。(c) 1997年。
The effects of nitric oxide-containing solution and different nitric oxide donors were investigated on spontaneously active neurons using extracellular recording technique in areas of rat spinal cord slices where high levels of nitric oxide synthase are present. In lamina X, 93% of all neurons investigated (n=84) increased their firing rate and 2% decreased it by superfusion with the nitric oxide donor sodium nitroprusside. In contrast, 49% of all neurons in laminae I and II (n=90) were inhibited and only 28% were activated. Both effects were due to the postsynaptic action of sodium nitroprusside, because they could still be observed in medium containing 0.3 mM Ca2+ and 9 mM Mg2+, known to block synaptic transmission. Application of 8-bromo-cyclic-GMP caused an excitation of every neuron which was excited by sodium nitroprusside and an inhibition of every cell which was inhibited by sodium nitroprusside (n=25). This effect was different from the effect of S-bromo-cyclic-AMP, which mimicked only the excitatory, but not the inhibitory response of sodium nitroprusside.These results provide evidence that nitric oxide in the spinal cord can directly cause an excitation or an inhibition of the electrical activity of spinal neurons. Another, more general conclusion from our results is that the nitric oxide-induced production of cyclic-GMP alone does not allow any prediction about an excitatory or inhibitory effect on the neuronal activity, which has to be determined separately. (C) 1997 IBRO.