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体外CA1区胆碱能θ振荡期间单个爆发诱导的双向突触可塑性。

Bidirectional synaptic plasticity induced by a single burst during cholinergic theta oscillation in CA1 in vitro.

作者信息

Huerta P T, Lisman J E

机构信息

Department of Biology, Brandeis University, Waltham, Massachusetts 02254, USA.

出版信息

Neuron. 1995 Nov;15(5):1053-63. doi: 10.1016/0896-6273(95)90094-2.

Abstract

In standard protocols, the frequency of synaptic stimulation determines whether CA1 hippocampal synapses undergo long-term potentiation or depression. Here we show that during cholinergically induced theta oscillation (theta) synaptic plasticity is greatly sensitized and can be induced by a single burst (4 pulses, 100 Hz). A burst given at the peak of theta induces homosynaptic LTP; the same burst at a trough induces homosynaptic LTD of previously potentiated synapses. Heterosynaptic LTD is produced at inactive synapses when others undergo LTP. The synaptic modifications during theta require NMDA receptors and muscarinic receptors. The enhancement is cooperative and occludes with standard LTP. These results suggest that the similar bursts observed during theta rhythm in vivo may be a natural stimulus for inducing LTP/LTD.

摘要

在标准实验方案中,突触刺激的频率决定了海马体CA1区突触是经历长时程增强还是长时程抑制。我们在此表明,在胆碱能诱导的theta振荡(theta)期间,突触可塑性大大增强,并且可以由单个爆发(4个脉冲,100赫兹)诱导产生。在theta峰值处给予的爆发诱导同突触长时程增强;在波谷处给予相同的爆发则诱导先前增强突触的同突触长时程抑制。当其他突触经历长时程增强时,在未激活的突触处产生异突触长时程抑制。theta期间的突触修饰需要NMDA受体和毒蕈碱受体。这种增强是协同性的,并且与标准长时程增强相互阻断。这些结果表明,在体内theta节律期间观察到的类似爆发可能是诱导长时程增强/长时程抑制的自然刺激。

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