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ACPD和AP3对体外培养的小脑薄片中浦肯野细胞平行纤维介导的兴奋性突触后电位的影响。

Effects of ACPD and AP3 on parallel-fibre-mediated EPSPs of Purkinje cells in cerebellar slices in vitro.

作者信息

Crepel F, Daniel H, Hemart N, Jaillard D

机构信息

Laboratoire de Neurobiologie et Neuropharmacologie du Développement, URA CNRS 1121, Université Paris-Sud, Orsay, France.

出版信息

Exp Brain Res. 1991;86(2):402-6. doi: 10.1007/BF00228964.

DOI:10.1007/BF00228964
PMID:1661680
Abstract

The effects of trans-1-amino-cyclopentyl-1,3-dicarboxylate (trans-ACPD) and of DL-2-amino-3-phosphonopropionic acid (AP3), i.e. selective agonist and antagonist of metabotropic quisqualate receptors respectively, on parallel fibre (PF)-mediated EPSPs of Purkinje cells (PCs) were studied in an in vitro slice preparation. Bath application of 500 microM trans-ACPD in conjunction with PF stimulation at 0.2 or 1 Hz depending on the cell always induced a marked depression of PF-mediated EPSPs, which was fully reversible in most cases after wash-out of this compound. Trans-ACPD also often induced a transient depolarization of PCs which induced calcium spike firing in these cells and which again no longer persisted after wash-out of trans-ACPD. Even in cells which were depolarized by trans-ACPD, the decrease in amplitude of PF-mediated EPSPs started before the appearance of calcium spikes, lasted longer than the transient depolarizing effect of trans-ACPD, and was accompanied by no variation in input resistance of the cells when they were manually clamped at their initial resting potential. Bath application of 600 microM DL-AP3 had no effect on PF-mediated EPSPs or the bioelectrical activities of PCs. Moreover, it did not prevent the effects of trans-ACPD mentioned before. The present results are not consistent with the view that coactivation of ionotropic and metabotropic quisqualate receptors of PCs is sufficient to induce a long-term depression of PF-mediated EPSPs.

摘要

在体外脑片制备中,研究了反式-1-氨基环戊基-1,3-二羧酸(反式-ACPD)和DL-2-氨基-3-膦酰丙酸(AP3)(分别为代谢型喹啉酸受体的选择性激动剂和拮抗剂)对浦肯野细胞(PCs)平行纤维(PF)介导的兴奋性突触后电位(EPSPs)的影响。根据细胞情况,在浴槽中应用500微摩尔的反式-ACPD并结合0.2或1赫兹的PF刺激,总能诱导PF介导的EPSPs明显抑制,在大多数情况下,洗脱该化合物后这种抑制是完全可逆的。反式-ACPD还经常诱导PCs短暂去极化,导致这些细胞产生钙峰放电,在洗脱反式-ACPD后这种情况也不再持续。即使在被反式-ACPD去极化的细胞中,PF介导的EPSPs幅度下降也在钙峰出现之前开始,持续时间比反式-ACPD的短暂去极化作用更长,并且当手动钳制细胞使其处于初始静息电位时,细胞的输入电阻没有变化。在浴槽中应用600微摩尔的DL-AP3对PF介导的EPSPs或PCs的生物电活动没有影响。此外,它不能阻止之前提到的反式-ACPD的作用。目前的结果与以下观点不一致,即PCs离子型和代谢型喹啉酸受体的共同激活足以诱导PF介导的EPSPs的长期抑制。

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