Crunelli V, Forda S, Kelly J S
J Physiol. 1984 Jun;351:327-42. doi: 10.1113/jphysiol.1984.sp015248.
The responses of granule cells to glutamate, aspartate, N-methyl-D-aspartate (NMDA), quisqualate and kainate applied by ionophoresis on to their dendrites in the middle molecular layer of the dentate gyrus were studied with intracellular electrodes using an in vitro hippocampal slice preparation. On passive depolarization 75% of the granule cells displayed anomalous rectification, which persisted in the presence of TTX and TEA but was eliminated by Co2+ or the intracellular injection of Cs+. Short ionophoretic applications of all the excitatory amino acids evoked dose-dependent depolarizations that were highly localized: movement of the ionophoretic electrode by as little as 10 microns could substantially change the size of the response. The depolarizations evoked by glutamate, asparatate, quisqualate and kainate were unaffected by TTX and Co2+. The depolarization evoked by NMDA was unaffected by TTX but markedly reduced by Co2+. Following intracellular injection of Cs+, neurones could be depolarized to +30 mV and the depolarizations produced by glutamate, quisqualate, NMDA and kainate reversed. The reversal potentials (E) were Eglutamate: -5.6 +/- 0.4 mV; ENMDA: 1.8 +/- 1.9 mV; Equisqualate: -3.9 +/- 1.9 mV; Ekainate: -4.6 +/- 2.0 mV. The excitatory post-synaptic potential (e.p.s.p.) evoked by stimulation of the medial perforant path could also be reversed and Ee.p.s.p. was -5.5 +/- 1.1 mV. The 6 mV difference between ENMDA and the equilibrium potential for the other exogenously applied excitatory amino acids and the statistically significant difference between ENMDA and Ee.p.s.p. (P less than 0.005; d.f.: 7) is consistent with our earlier hypothesis that both the transmitter released by the medial perforant path and exogenously applied glutamate are unlikely to interact with NMDA receptors.
采用细胞内电极，利用海马脑片制备技术，研究了离子电泳施加于齿状回中层分子层颗粒细胞树突上的谷氨酸、天冬氨酸、N - 甲基 - D - 天冬氨酸（NMDA）、quisqualate和海人藻酸所引起的反应。在被动去极化时，75%的颗粒细胞表现出反常整流，在存在河豚毒素（TTX）和四乙铵（TEA）时这种现象持续存在，但可被Co2 +或细胞内注射Cs +消除。所有兴奋性氨基酸的短时间离子电泳施加均引起剂量依赖性去极化，且高度局限：离子电泳电极移动仅10微米就能显著改变反应大小。谷氨酸、天冬氨酸、quisqualate和海人藻酸所引起的去极化不受TTX和Co2 +影响。NMDA所引起的去极化不受TTX影响，但被Co2 +显著降低。细胞内注射Cs +后，神经元可被去极化至+30 mV，谷氨酸、quisqualate、NMDA和海人藻酸所产生的去极化发生反转。反转电位（E）分别为：E谷氨酸：-5.6±0.4 mV；ENMDA：1.8±1.9 mV；E quisqualate：-3.9±1.9 mV；E海人藻酸：-4.6±2.0 mV。刺激内侧穿通通路所诱发的兴奋性突触后电位（e.p.s.p.）也可被反转，Ee.p.s.p.为-5.5±1.1 mV。ENMDA与其他外源性施加的兴奋性氨基酸的平衡电位之间6 mV的差异以及ENMDA与Ee.p.s.p.之间具有统计学意义的差异（P＜0.005；自由度：7）与我们早期的假设一致，即内侧穿通通路释放的递质和外源性施加的谷氨酸都不太可能与NMDA受体相互作用。
