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兴奋性氨基酸可抑制新生大鼠交感神经节前神经元的突触电流。

Excitatory amino acids depress synaptic currents in neonate rat sympathetic preganglionic neurons.

作者信息

Wu S Y, Dun N J

机构信息

Department of Anatomy, Medical College of Ohio, Toledo 43699.

出版信息

J Neurophysiol. 1993 Jun;69(6):2030-8. doi: 10.1152/jn.1993.69.6.2030.

Abstract
  1. Whole-cell patch-clamp recordings were made from sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices of 10- to 16-day-old rats, and the effects of L-glutamate (L-Glu) and analogues on excitatory (EPSCs) and inhibitory (IPSCs) postsynaptic currents evoked by stimulation of lateral funiculus were studied. 2. L-Glu (10-300 microM), quisqualate (QA, 0.1-3 microM), kainate (KA, 0.3-10 microM), ibotenate (10-25 microM), and L-2-amino-4-phosphonobutyrate (L-AP4, 25-300 microM) depressed the EPSCs and IPSCs in a concentration-dependent manner, the rank order being QA > KA > ibotenate > L-AP4 > or = L-Glu. The metabotropic glutamate receptor agonist trans-1-amino-1,3-cyclopentane-dicarboxylic acid (trans-ACPD, 25-100 microM) reduced the synaptic currents as well. A similar effect was not observed with N-methyl-D-aspartate (NMDA). 3. The excitatory amino acid uptake inhibitor L-aspartic acid-beta-hydroxamate (AAH, 100 microM), although having little or no direct effect on EPSCs, unmasked the inhibitory effect of low (< or = 1 microM) concentrations of L-Glu. 4. The synaptic depression was not accompanied by a detectable change in holding currents or EPSC reversal potentials and decay constants in the majority of SPNs studied. At higher concentrations, L-Glu and analogues, but not L-AP4, induced an inward current in some SPNs. 5. Although strongly depressing the EPSCs, L-AP4 and trans-ACPD had no significant effect on the amplitude of inward current induced by exogenous L-Glu.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 采用全细胞膜片钳记录技术,从10至16日龄大鼠胸腰段脊髓横切片中的交感神经节前神经元(SPN)进行记录,研究了L-谷氨酸(L-Glu)及其类似物对刺激外侧索诱发的兴奋性(EPSCs)和抑制性(IPSCs)突触后电流的影响。2. L-Glu(10 - 300微摩尔)、quisqualate(QA,0.1 - 3微摩尔)、kainate(KA,0.3 - 10微摩尔)、ibotenate(10 - 25微摩尔)和L-2-氨基-4-膦酸丁酸(L-AP4,25 - 300微摩尔)以浓度依赖的方式抑制EPSCs和IPSCs,其顺序为QA > KA > ibotenate > L-AP4 > 或 = L-Glu。代谢型谷氨酸受体激动剂反式-1-氨基-1,3-环戊烷二羧酸(反式-ACPD,25 - 100微摩尔)也降低了突触电流。N-甲基-D-天冬氨酸(NMDA)未观察到类似效应。3. 兴奋性氨基酸摄取抑制剂L-天冬氨酸-β-羟肟酸(AAH,100微摩尔)虽然对EPSCs几乎没有直接影响,但揭示了低(≤1微摩尔)浓度L-Glu的抑制作用。4. 在大多数研究的SPN中,突触抑制并未伴随可检测到的钳制电流、EPSC反转电位和衰减常数的变化。在较高浓度下,L-Glu及其类似物,但不是L-AP4,在一些SPN中诱导了内向电流。5. 尽管L-AP4和反式-ACPD强烈抑制EPSCs,但对由外源性L-Glu诱导的内向电流幅度没有显著影响。(摘要截断于250字)

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