Calabresi P, De Murtas M, Mercuri N B, Bernardi G
Clinica Neurologica, 2a Università di Roma, Italy.
J Neurosci. 1990 Dec;10(12):3960-9. doi: 10.1523/JNEUROSCI.10-12-03960.1990.
The electrophysiological effects produced by different concentrations of kainic acid (KA) were studied by utilizing intracellular recordings from neostriatal slices. In most of the recorded cells (81%), concentrations of KA ranging between 10 and 300 nM produced reversible and dose-dependent membrane depolarizations. Higher concentrations of this agonist caused larger depolarizations and changes of the membrane properties of the recorded neurons not reversible during the time of recording. In a smaller percentage (19%) of the recorded cells, 10-100 nM KA did not produce significant membrane depolarizations; in these neurons, the depolarizations produced by higher concentrations of KA were small and reversible. The 2 populations of neurons showed similar electrophysiological properties and did not reveal differential sensitivity to quisqualic acid (QUIS; 10-30 microM) or to NMDA (10-30 microM). Tetrodotoxin (TTX; 1 microM) did not reduce the depolarizations produced by KA and by NMDA. Low-calcium, cobalt-containing solutions abolished the effects produced by NMDA, but not the KA-induced depolarizations. Kynurenic acid (500 microM) significantly antagonized the depolarizations produced by KA and reduced the changes of the membrane properties caused by high doses of this agonist. In several neurons, KA induced bicuculline-sensitive synaptic depolarizing potentials. Our findings suggest the presence of 2 subpopulations of neostriatal neurons showing differential postsynaptic sensitivity to KA. The differential sensitivity of neostriatal neurons to KA might influence the responses of these cells to glutamatergic cortical inputs and the degenerative changes observed in neostriatal neurons in some pathological conditions.
利用新纹状体切片的细胞内记录技术,研究了不同浓度的海人酸(KA)所产生的电生理效应。在大多数被记录的细胞(81%)中,浓度在10至300纳摩尔之间的KA可产生可逆的、剂量依赖性的膜去极化。该激动剂的较高浓度会导致更大的去极化以及所记录神经元膜特性的改变,在记录期间这些改变是不可逆的。在较小比例(19%)的被记录细胞中,10 - 100纳摩尔的KA并未产生显著的膜去极化;在这些神经元中,较高浓度的KA所产生的去极化较小且可逆。这两类神经元表现出相似的电生理特性,并且对 quisqualic 酸(QUIS;10 - 30微摩尔)或NMDA(10 - 30微摩尔)未显示出不同的敏感性。河豚毒素(TTX;1微摩尔)并未降低KA和NMDA所产生的去极化。低钙、含钴溶液消除了NMDA所产生的效应,但未消除KA诱导的去极化。犬尿氨酸(500微摩尔)显著拮抗KA所产生的去极化,并减少了高剂量该激动剂引起的膜特性变化。在一些神经元中,KA诱导了荷包牡丹碱敏感的突触去极化电位。我们的研究结果表明存在两类新纹状体神经元亚群,它们对KA表现出不同的突触后敏感性。新纹状体神经元对KA的不同敏感性可能会影响这些细胞对谷氨酸能皮质输入的反应以及在某些病理条件下新纹状体神经元中观察到的退行性变化。