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蛙视顶盖中层的反复谷氨酸能兴奋受到毒蕈碱抑制,防止 NMDA 受体在传出神经元上激活。

Muscarinic inhibition of recurrent glutamatergic excitation in frog tectum column prevents NMDA receptor activation on efferent neuron.

机构信息

Laboratory of Neurophysiology, Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, 50009 Kaunas, Lithuania.

出版信息

Exp Brain Res. 2011 Feb;208(3):323-34. doi: 10.1007/s00221-010-2484-z. Epub 2010 Nov 17.

Abstract

It is widely recognized that neuronal network activity can be modulated via activation of nicotinic and muscarinic acetylcholine receptors located pre- and postsynaptically. It was established in our earlier study that the activation of presynaptic nicotinic receptors greatly facilitates the retinotectal glutamatergic transmission. In the present study, we have determined a transmitter of tectal recurrent excitation and explored the effects of muscarinic acetylcholine receptor activation on the recurrent excitation and the activity of frog tectum column in vivo. Discharge of a single retinal ganglion cell was elicited by a minimal electrical stimulation of the retina. Evoked activity of the tectum column was recorded using the carbon-fiber microelectrode inserted into the tectum layer F. We found the following: 1. The recurrent excitation in the tectum column was not affected by d-tubocurarine (10 μM) and was greatly depressed by the kynurenic acid (500 μM), demonstrating glutamatergic nature of the recurrent excitation. 2. The glutamatergic recurrent excitation was largely reduced by carbamylcholine (100 μM) and oxotremorine-M (10 μM), demonstrating that the activation of muscarinic receptors, located, presumably, on the presynaptic terminals of recurrent pear-shaped neurons, inhibits the recurrent excitation in the tectum column. 3. The muscarinic inhibition of glutamatergic recurrent transmission had critical influence on the activity of the tectum column, preventing the generation of an output signal through suppression of the NMDA receptor activation and establishing necessary conditions for returning of the network to its resting state.

摘要

人们普遍认为,神经元网络的活动可以通过激活位于突触前和突触后的烟碱和毒蕈碱乙酰胆碱受体来调节。在我们之前的研究中已经确定,激活突触前烟碱受体可以极大地促进视网膜-顶盖谷氨酸能传递。在本研究中,我们确定了顶盖内反射兴奋的递质,并探讨了毒蕈碱乙酰胆碱受体激活对顶盖内反射兴奋和青蛙顶盖柱活性的影响。通过对视网膜的最小电刺激来诱发单个视网膜神经节细胞的放电。使用插入到 F 层的碳纤维微电极记录顶盖柱的诱发电活动。我们发现:1. 顶盖柱内的内反射兴奋不受 d-筒箭毒碱(10μM)的影响,但被烟碱酸(500μM)大大抑制,表明内反射兴奋的谷氨酸能性质。2. 谷氨酸能内反射兴奋被氨基甲酰胆碱(100μM)和 oxotremorine-M(10μM)大大减少,表明位于可能位于内反射梨形神经元突触前末梢的毒蕈碱受体的激活抑制了顶盖柱内的内反射兴奋。3. 谷氨酸能内反射传递的毒蕈碱抑制对顶盖柱的活动有重要影响,通过抑制 NMDA 受体的激活来抑制输出信号的产生,并为网络返回其静息状态建立必要条件。

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