CHARACTERIZATION OF A SLOW CHOLINERGIC POST-SYNAPTIC POTENTIAL RECORDED INVITRO FROM RAT HIPPOCAMPAL PYRAMIDAL CELLS
CHARACTERIZATION OF A SLOW CHOLINERGIC POST-SYNAPTIC POTENTIAL RECORDED INVITRO FROM RAT HIPPOCAMPAL PYRAMIDAL CELLS
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DOI：
10.1113/jphysiol.1984.sp015285
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发表时间：
1984-01-01
影响因子：
5.5
通讯作者：
NICOLL, RA
中科院分区：
文献类型：
--
作者：
COLE, AE;NICOLL, RA
海马切片制备中 CA1 锥体细胞的细胞内记录用于比较外源性乙酰胆碱 (ACh) 和拟胆碱药物的作用与切片中已知含有胆碱能纤维的电刺激位点的作用。 ACh 使锥体细胞去极化，并伴随输入电阻的增加，阻断 Ca 激活的 K 电导 (GK(Ca))，并阻断动作电位放电的调节。所有这些作用都被毒蕈碱拮抗剂阿托品阻断。对东方层的重复电刺激引起一系列快速兴奋性突触后电位（EPSP），随后是抑制性突触后电位。这些电位之后是持续 20-30 秒的缓慢 EPSP。缓慢的 EPSP 被丝氨酸选择性增强并被阿托品阻断。 ACh 的离子电渗应用密切模仿了缓慢 EPSP 的时间进程。缓慢的 EPSP 被河豚毒素和 Cd 阻断，表明它依赖于传播的动作电位和 Ca。与引发较早的突触电位相比，引发缓慢的 EPSP 需要更高的刺激强度。重复刺激后慢 EPSP 的大小显着增加。刺激肺泡，s。奥里安斯锥体和菌毛均诱发缓慢的 EPSP，而 s 的刺激。辐射相对无效。在缓慢的 EPSP 过程中，电池的输入电阻增加。细胞超极化会减小慢速 EPSP 的大小，并且在 -70 mV 或更高的膜电位下，几乎没有记录到反应。刺激 s。 Oriens 阻断 GK(Ca) 和动作电位放电的调节。这些效应可以在膜电位没有任何变化的情况下观察到，并被丝氨酸增强并被阿托品阻断。电生理学结果表明，CA1 锥体细胞接收胆碱能输入，并证明这种输入可以在对膜电位没有任何明显影响的情况下，在数十秒内显着改变这些神经元的放电特性。这种行为与先前描述的大脑该区域的突触电位形成鲜明对比。
Intracellular recording from CA1 pyramidal cells in the hippocampal slice preparation was used to compare the action of exogenously applied acetylcholine (ACh) and cholinomimetics to the effect of electrically stimulating sites in the slice known to contain cholinergic fibers. ACh depolarized pyramidal cells with an associated increase in input resistance, blocked a Ca-activated K conductance (GK(Ca)), and blocked accommodation of action potential discharge. All of these actions were blocked by the muscarinic antagonist, atropine. Repetitive electrical stimulation of stratum (s.) oriens evoked a series of fast excitatory post-synaptic potentials (EPSP) followed by an inhibitory post-synaptic potential. These potentials were followed by a slow EPSP that lasted 20-30 s. The slow EPSP was selectively enhanced by eserine and blocked by atropine. Ionophoretic application of ACh closely mimicked the time course of the slow EPSP. The slow EPSP was blocked by tetrodotoxin and Cd, indicating that it was dependent on propagated action potentials and on Ca. Considerably higher stimulus strengths were needed to elicit a slow EPSP than to elicit the earlier synaptic potentials. The size of the slow EPSP was markedly increased by repetitive stimulation. Stimulation of the alveus, s. oriens, s. pyramidale and fimbria all evoked a slow EPSP, while stimulation of s. radiatum was relatively ineffective. The input resistance of the cell increased during the slow EPSP. Hyperpolarizing the cell decreased the size of the slow EPSP and at membrane potentials of -70 mV or greater, little response was recorded. Stimulation of s. oriens blocked GK(Ca) and accommodation of action potential discharge. These effects, which could be seen in the absence of any change in membrane potential, were enhanced by eserine and blocked by atropine. The electrophysiological results establish that CA1 pyramidal cells receive a cholinergic input and demonstrate that this input can dramatically alter the firing properties of these neurons for tens of seconds in the absence of any marked effect on membrane potential. Such an action contrasts with previously characterized synaptic potentials in this region of the brain.