Properties of carbachol-induced oscillatory activity in rat hippocampus.
Properties of carbachol-induced oscillatory activity in rat hippocampus.
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DOI：
10.1152/jn.1997.78.5.2631
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发表时间：
1997-11
影响因子：
2.5
通讯作者：
John H. Williams;J. Kauer
中科院分区：
文献类型：
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作者：
John H. Williams;J. Kauer
卡巴胆碱诱导的大鼠海马振荡活动的特性。 J.神经生理学。 78: 2631-2640, 1997。最近人们对卡巴胆碱振荡作为海马 θ 节律体外模型的兴趣重新兴起，促使我们评估所涉及的电路机制。在细胞外记录中，在存在卡巴胆碱的情况下，在 CA3 和 CA1 子场中观察到场电位的规则间隔的爆发模式。去除 CA3 区域消除了在 CA1 中观察到的振荡活动，表明振荡发生器位于 CA3 中。 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸 (AMPA) 受体拮抗剂 6,7-二硝基喹喔啉-2,3-二酮 (DNQX) 可阻断卡巴胆碱振荡，表明 AMPA 受体介导的突触电流对于群体振荡是必需的。此外，振荡活性传播到 CA1 需要完整的 N-甲基-天冬氨酸受体。这些数据与癫痫样爆发比与体内描述的θ节律更一致。在存在卡巴胆碱的情况下，单个 CA3 锥体细胞表现出缓慢、有节奏的内在振荡，这种振荡不会被 DNQX 阻断，并且会因膜超极化而增强。我们假设这种较慢的振荡是通过刺激多个突触连接的 CA3 神经元参与触发群体振荡的基本振荡器。 γ-氨基丁酸-A (GABAA) 受体对于卡巴胆碱引发同步 CA3 场事件不是必需的，但对于观察到的爆发模式至关重要。 GABAB 和代谢型谷氨酸受体似乎都不是卡巴胆碱振荡所必需的。然而，烟碱型以及 M1 和 M3 毒蕈碱型胆碱能受体都有助于这种活性的产生。这些结果建立了有助于卡巴胆碱诱导的振荡的局部电路元件和神经递质受体，并表明卡巴胆碱诱导的振荡与体内的θ节律根本不同。
Properties of carbachol-induced oscillatory activity in rat hippocampus. J. Neurophysiol. 78: 2631-2640, 1997. The recent resurgence of interest in carbachol oscillations as an in vitro model of theta rhythm in the hippocampus prompted us to evaluate the circuit mechanisms involved. In extracellular recordings, a regularly spaced bursting pattern of field potentials was observed in both CA3 and CA1 subfields in the presence of carbachol. Removal of the CA3 region abolished oscillatory activity observed in CA1, suggesting that the oscillatory generator is located in CA3. An alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), blocked carbachol oscillations, indicating that AMPA receptor-mediated synaptic currents are necessary for the population oscillation. Moreover, the spread of oscillatory activity into CA1 required intact N-methyl--aspartate receptors. These data are more consistent with epileptiform bursting than with theta rhythm described in vivo. In the presence of carbachol, individual CA3 pyramidal cells exhibited a slow, rhythmic intrinsic oscillation that was not blocked by DNQX and that was enhanced by membrane hyperpolarization. We hypothesize that this slower oscillation is the fundamental oscillator that participates in triggering the population oscillation by exciting multiple synaptically connected CA3 neurons. gamma-aminobutyric acid-A (GABAA) receptors are not necessary for carbachol to elicit synchronous CA3 field events but are essential to the bursting pattern observed. Neither GABAB nor metabotropic glutamate receptors appear to be necessary for carbachol oscillations. However, both nicotinic and M1 and M3 muscarinic cholinergic receptors contribute to the generation of this activity. These results establish the local circuit elements and neurotransmitter receptors that contribute to carbachol-induced oscillations and indicate that carbachol-induced oscillations are fundamentally distinct from theta rhythm in vivo.