The properties of carbachol-induced beta oscillation in rat hippocampal slices

The properties of carbachol-induced beta oscillation in rat hippocampal slices
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DOI:
10.1016/j.neures.2005.10.011
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发表时间:
2006-02-01
影响因子:
2.9
通讯作者:
Natsume, K
Natsume, K
中科院分区:
医学4区
文献类型:
--
作者:
Arai, J;Natsume, K

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利用大鼠海马切片研究了碳巴酚诱导的β振荡的节律性和药理学性质。施用30 μ M苯酚,在CA3区记录到频率为13-20 Hz的β范围振荡。一种AMPA受体拮抗剂CNQX可以减弱这种振荡。一种NMDA受体拮抗剂APV显著抑制了预先建立的β振荡。预施用APV阻断了碳酚诱导的β振荡的开始。当GABA(a)受体拮抗剂bicuculline (BIC)应用于预先建立的β振荡时,频率降低到θ范围。当5 μ M BIC与30 μ M苯酚共同作用时,β振荡未开始;相反,类似θ的活动被诱导。据报道,海马切片中的氨基酚可以诱导不受BIC调节的类theta活动,而BIC则促进活动的开始。本研究结果表明,GABAA受体介导的抑制性传递调节了β振荡,并且该传递是振荡启动过程所必需的。因此,碳甾醇诱导的β振荡的开始和产生机制将不同于碳甾醇诱导的β样活性。(c) 2005爱思唯尔爱尔兰有限公司和日本神经科学学会。版权所有。
The rhythmical and pharmacological properties of carbachol-induced beta oscillation were Studied using rat hippocampal slices. With the application of 30 mu M carbachol, beta-range oscillations with frequencies of 13-20 Hz were recorded from the CA3 region. An AMPA receptor antagonist, CNQX, diminished the oscillations. An NMDA receptor antagonist, APV, significantly suppressed the pre-established beta oscillations. The pre-application of APV blocked the start of the carbachol-induced beta oscillations. When bicuculline (BIC), a GABA(A) receptor antagonist, was applied to the pre-established beta oscillations, the frequency decreased to the theta-range. When 5 mu M BIC was applied with 30 mu M carbachol, the beta oscillations did not start; instead, theta-like activities were induced. It has been reported that carbachol in hippocampal slices can induce theta-like activities, which are not modulated by BIC, while BIC's facilitating the start of the activities. The results of the present study suggest that the GABAA receptor-mediated inhibitory transmission modulates the beta oscillation and that the transmission is needed for the start process of the oscillations. Therefore, the start and generation mechanisms of carbachol-induced beta oscillation will be different from those of carbachol-induced theta-like activities. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.