Fox S E
Department of Physiology, State University of New York, Brooklyn 11203.
Exp Brain Res. 1989;77(2):283-94. doi: 10.1007/BF00274985.
Intracellular recordings were made from hippocampal pyramidal cells identified by their depths and their responses to commissural stimulation. Recordings were made during spontaneous bouts of hippocampal theta rhythm in urethane anesthetized rats. Membrane potentials (Vm) of pyramidal cells varied with the phase of the theta rhythm, that is, there was an "intracellular theta rhythm". The changes in Vm averaged about 2 mV peak to peak. Averaged intracellular theta waves showed that CA1 pyramids were most depolarized at the time of the positive peak of the extracellular theta rhythm recorded in (and superficial to) the CA1 pyramidal cell layer (CA1 theta). Peak depolarizations for CA3/4 pyramids were more broadly distributed, but occurred mainly in the interval just before the positive peak to just before the negative peak of the CA1 theta. Input impedance minima that were measurable at frequencies as high as 100 Hz occurred at about the same phases of the extracellular theta rhythm as the peak depolarizations (positive-going zero crossing to negative-going zero crossing of the CA1 theta). Such impedance changes imply conductance changes on the soma. The magnitude and localization of the conductance changes suggests that somatic IPSPs make major contributions to the intracellular theta rhythm. The phase relation between the intracellular and extracellular theta rhythms could be reversed by long duration current pulses that depolarized the cells slightly. This implies that either the intracellular theta-related IPSPs are depolarizing potential changes, or that they occur simultaneously with EPSPs. The phase of the intracellular theta rhythm was generally unaffected by long duration hyperpolarizing current pulses. Chloride leakage that reversed the evoked IPSPs usually had no effect on the phase of the intracellular theta rhythm, although in one case it appeared to cause its amplitude to increase.
通过海马锥体细胞的深度及其对联合刺激的反应来识别这些细胞，并对其进行细胞内记录。记录是在氨基甲酸乙酯麻醉的大鼠海马θ节律的自发发作期间进行的。锥体细胞的膜电位（Vm）随θ节律的相位而变化，也就是说，存在“细胞内θ节律”。Vm的变化峰峰值平均约为2 mV。平均细胞内θ波显示，CA1锥体神经元在CA1锥体细胞层（CA1θ）记录到的（以及该层表面的）细胞外θ节律的正峰时去极化程度最高。CA3/4锥体神经元的峰值去极化分布更广泛，但主要发生在CA1θ的正峰之前到负峰之前的时间段内。在高达100 Hz的频率下可测量的输入阻抗最小值出现在细胞外θ节律的与峰值去极化相同的相位（CA1θ从正向过零到负向过零）。这种阻抗变化意味着体细胞的电导变化。电导变化的幅度和定位表明，体细胞抑制性突触后电位（IPSPs）对细胞内θ节律有主要贡献。细胞内和细胞外θ节律之间的相位关系可以通过使细胞轻微去极化的长时间电流脉冲来逆转。这意味着要么细胞内与θ相关的IPSPs是去极化电位变化，要么它们与兴奋性突触后电位（EPSPs）同时发生。细胞内θ节律的相位通常不受长时间超极化电流脉冲的影响。使诱发的IPSPs反转的氯离子泄漏通常对细胞内θ节律的相位没有影响，尽管在一个案例中它似乎导致其幅度增加。
