Zeise M L, Knöpfel T, Zieglgänsberger W
Clinical Neuropharmacology, Max-Planck-Institute for Psychiatry, München, F.R.G.
Brain Res. 1988 Mar 8;443(1-2):373-6. doi: 10.1016/0006-8993(88)91636-8.
The effect of (+/-)-beta-parachlorophenylglutamate (CP) on depolarizations induced by iontophoretically applied L-glutamate, L-aspartate, L-homocysteate (L-HCA) and D-HCA was investigated in neurons of the rat neocortex in vitro. CP, a reported blocker of amino acid uptake, strongly enhanced L-HCA responses whereas responses to the other amino acids remained little affected. This action was observed irrespective of whether CP was administered iontophoretically or pneumatically from micropipettes. CP (5 mM) administered alone had no effect on membrane potential. These findings suggest the existence of a specific uptake system for L-HCA providing further evidence in favour of a possible function of L-HCA as an endogenous ligand for the N-methyl-D-aspartate receptor in the rat neocortex.
在体外对大鼠新皮质神经元进行研究，考察了（±）-β-对氯苯基谷氨酸（CP）对离子导入L-谷氨酸、L-天冬氨酸、L-同型半胱氨酸（L-HCA）和D-同型半胱氨酸（D-HCA）所诱导的去极化的影响。据报道，CP是一种氨基酸摄取阻滞剂，它能显著增强L-HCA反应，而对其他氨基酸的反应影响很小。无论CP是通过离子导入还是从微量移液器气动给药，均观察到这种作用。单独给予CP（5 mM）对膜电位无影响。这些发现提示存在一种L-HCA特异性摄取系统，为L-HCA作为大鼠新皮质中N-甲基-D-天冬氨酸受体的内源性配体的可能功能提供了进一步的证据。
