Taube J S, Schwartzkroin P A
Neurosci Lett. 1987 Jul 9;78(1):85-90. doi: 10.1016/0304-3940(87)90566-0.
Micropressure injection of glutamate onto the apical dendrites of hippocampal CA1 pyramidal cells usually produces a fast rising, brief depolarization. However, hyperpolarizing responses with longer durations (300-500 ms) can be produced over a range of drug electrode locations. These hyperpolarizations can be reversed with intracellular injection of hyperpolarizing current. Localized application of glutamate in the stratum radiatum produces a depolarizing response in intracellularly recorded CA1 interneurons. Previous studies have shown that the dendrites of GABA-ergic basket cell interneurons extend into the stratum radiatum and are involved in mediating feedforward inhibition of pyramidal neurons. The glutamate-induced hyperpolarizations observed in pyramidal neurons are probably due to direct excitation of dendrites of interneurons, which in turn produce a synaptic inhibition in pyramidal cells.
将谷氨酸微量注射到海马体CA1锥体细胞的顶端树突上，通常会产生快速上升的短暂去极化。然而，在一系列药物电极位置上可产生持续时间更长（300 - 500毫秒）的超极化反应。这些超极化可通过细胞内注射超极化电流来逆转。在辐射层局部应用谷氨酸会在细胞内记录的CA1中间神经元中产生去极化反应。先前的研究表明，γ-氨基丁酸能篮状细胞中间神经元的树突延伸到辐射层，并参与介导锥体细胞的前馈抑制。在锥体细胞中观察到的谷氨酸诱导的超极化可能是由于中间神经元树突的直接兴奋，进而在锥体细胞中产生突触抑制。
