SYNAPTIC AND INTRINSIC RESPONSES OF MEDIAL ENTORHINAL CORTICAL-CELLS IN NORMAL AND MAGNESIUM-FREE MEDIUM INVITRO
SYNAPTIC AND INTRINSIC RESPONSES OF MEDIAL ENTORHINAL CORTICAL-CELLS IN NORMAL AND MAGNESIUM-FREE MEDIUM INVITRO
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DOI：
10.1152/jn.1988.59.5.1476
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发表时间：
1988-05-01
影响因子：
2.5
通讯作者：
HEINEMANN, U
中科院分区：
文献类型：
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作者：
JONES, RSG;HEINEMANN, U
1.细胞外记录取体外培养的海马区及海马区旁脑片。刺激小脑下丘后，在内嗅皮层记录到的场电位与活体观察到的类似。2.脑片中镁的洗脱导致了类似于活体持续癫痫发作时的阵发性事件。这些事件在内侧内嗅皮层的IV/V层的波幅和持续时间最大，既可以自发发生，也可以是对丘下刺激的反应。切断海马体和内嗅觉皮质之间的连接并不能防止自发的癫痫样事件，但这种操作可以阻止齿状回中发生的更小、更短的事件。N-甲基-D-天冬氨酸(NMDA)受体拮抗剂DL-2-氨基-5-磷酸戊酸(2-AP5)可阻断自发和诱发的阵发性事件。3.细胞内记录显示IV/V层神经元。在大多数细胞内注入去极化电流，可诱发出一系列非衰减性动作电位，仅有微弱的峰频率调节，很少或根本没有后超极化。4.少量细胞在正电去极化时表现出猝发反应。爆发由缓慢的去极化和叠加的动作电位组成，在放电过程中幅度降低，持续时间延长。脉冲串由强烈的后超极化终止，此后，在延长的电流脉冲期间，出现了一系列持续不减的尖峰。如果细胞被保持在超极化水平，则猝发反应仍然存在，但通过保持细胞在去极化水平，突发反应被灭活。5.刺激下丘脑底核可诱发去极化突触电位。延迟和延长的去极化随着膜的超极化而明显减少，偶尔随去极化而增加。6.冲刷切片中的镁导致了晚期去极化的增强，并逆转了其电压依赖性。最终，对下丘脑的一次电击引起了与膜电导大幅增加相关的大的阵发性去极化。类似的事件在所有被测试的细胞中自发发生。阵发性去极化，无论是自发的还是诱发的，都被2-AP5迅速阻断。7.内侧内嗅觉皮质细胞具有多种固有和突触特性，极易产生持续性惊厥活动。癫痫发作事件的同步和放大可能依赖于NMDA型兴奋性氨基酸受体的存在，NMDA型受体似乎介导了深层细胞长时间的突触去极化。
1. Extracellular recordings were made from slices of hippocampus plus parahippocampal regions maintained in vitro. Field potentials, recorded in the entorhinal cortex after stimulation in the subiculum, resembled those observed in vivo. 2. Washout of magnesium from the slices resulted in paroxysmal events which resembled those occurring during sustained seizures in vivo. These events were greatest in amplitude and duration in layers IV/V of the medial entorhinal cortex and could occur both spontaneously and in response to subicular stimulation. Spontaneous seizure-like events were not prevented by severing the connections between the hippocampus and entorhinal cortex, but much smaller and shorter events occurring in the dentate gyrus were stopped by this manipulation. Both spontaneous and evoked paroxysmal events were blocked by perfusion with the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonovalerate (2-AP5). 3. Neurons in layers IV/V were characterized by intracellular recording. Injection of deploarizing current in most cells evoked a train of nondecrementing action potentials with only weak spike frequency accommodation and little or no posttrain afterhyperpolarization. 4. A small number of cells displayed burst response when depolarized by positive current. The burst consisted of a slow depolarization with superimposed action potentials which decreased in amplitude and increased in duration during the discharge. The burst was terminated by a strong afterhyperpolarization and thereafter, during prolonged current pulses a train of nondecrementing spikes occurred. The burst response remained if the cell was held at hyperpolarized levels but was inactivated by holding the cell at a depolarized level. 5. Depolarizing synaptic potentials could be evoked by stimulation in the subiculum. A delayed and prolonged depolarization clearly decremented with membrane hyperpolarization and, occasionally, increased with depolarization. 6. Washout of magnesium from the slices resulted in an enhancement of the late depolarization and a reversal of its voltage dependence. Eventually a single shock to the subiculum evoked a large all-or-none paroxysmal depolarization associated with a massive increase in membrane conductance. Similar events occurred spontaneously in all cells tested. The paroxysmal depolarizations, both spontaneous and evoked, were rapidly blocked by 2-AP5. 7. It is concluded that medial entorhinal cortical cells possess several intrinsic and synaptic properties which confer an extreme susceptibility to generation of sustained seizure activity. Synchronization and amplification of seizure events may depend on the presence of excitatory amino acid receptors of the NMDA-type, which appear to mediate a prolonged synaptic depolarization of cells in the deep layers.