Peet M J, Gregersen H, McLennan H
Neuroscience. 1986 Mar;17(3):635-41. doi: 10.1016/0306-4522(86)90036-9.
Intracellular recordings from pyramidal neurones during microiontophoretic ejection of N-methyl-D-aspartate and quisqualate into the pyramidal cell layer of the CA1 region of the rat hippocampal slice showed that both amino acids caused depolarization and evoked spike activity. Whereas quisqualate evoked tetrodotoxin-sensitive spikes, those produced by N-methyl-D-aspartate consisted of bursts of tetrodotoxin-sensitive action potentials superimposed on an underlying depolarizing shift of membrane potential. Both membrane depolarization and the superimposed depolarizing shifts associated with N-methyl-D-aspartate excitation were selectively and reversibly antagonized by the D(-) isomer of 2-amino-5-phosphonovalerate and Co2+. Both amino acids caused an increase in membrane conductance when small ejection currents were used, and the depolarizing response to these compounds was prevented by current injection. However, only the increase by N-methyl-D-aspartate was blocked by 2-amino-5-phosphonovalerate and Co2+. These results provide evidence to support the suggestion that different mechanisms underlie the excitatory response to N-methyl-D-aspartate and quisqualate in CA1 pyramidal neurones.
在将N-甲基-D-天冬氨酸和喹啉酸微量离子导入大鼠海马切片CA1区锥体细胞层的过程中,对锥体细胞进行细胞内记录,结果显示这两种氨基酸都会引起去极化并诱发锋电位活动。喹啉酸诱发的是对河豚毒素敏感的锋电位,而N-甲基-D-天冬氨酸产生的锋电位则是由河豚毒素敏感的动作电位爆发叠加在膜电位的基础去极化偏移上。与N-甲基-D-天冬氨酸兴奋相关的膜去极化和叠加的去极化偏移都被2-氨基-5-磷酸戊酸的D(-)异构体和Co2+选择性且可逆地拮抗。当使用小的离子导入电流时,这两种氨基酸都会导致膜电导增加,并且通过电流注入可阻止对这些化合物的去极化反应。然而,只有N-甲基-D-天冬氨酸引起的增加被2-氨基-5-磷酸戊酸和Co2+阻断。这些结果提供了证据,支持在CA1锥体细胞中对N-甲基-D-天冬氨酸和喹啉酸的兴奋性反应存在不同机制这一观点。