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低频刺激在成年麻醉和清醒大鼠海马体中可诱导同突触去极化增强,但不会诱导突触传递的长时程抑制。

Low-frequency stimulation induces homosynaptic depotentiation but not long-term depression of synaptic transmission in the adult anaesthetized and awake rat hippocampus in vivo.

作者信息

Doyle C A, Cullen W K, Rowan M J, Anwyl R

机构信息

Department of Physiology, Trinity College, Dublin, Ireland.

出版信息

Neuroscience. 1997 Mar;77(1):75-85. doi: 10.1016/s0306-4522(96)00427-7.

DOI:10.1016/s0306-4522(96)00427-7
PMID:9044376
Abstract

The induction of homosynaptic long-term depression and depotentiation of previously established long-term potentiation was investigated in the CA1 hippocampal region of anaesthetized and awake adult rats following prolonged ipsilateral low-frequency stimulation of the Schaffer collateral/ commissural pathway. Prolonged low-frequency stimulation at 1-10 Hz failed to induce long-term depression of field excitatory postsynaptic potentials in the anaesthetized or awake adult rat. However, prolonged low-frequency stimulation at 5 and 10 Hz, although not at 1 or 2 Hz, did induce depotentiation of previously established long-term potentiation in anaesthetized animals. Thus, in the anaesthetized animals, 900 pulses at 10 Hz induced a depotentiation of 68%, 59% and 66% when given 10, 30 and 40 min following long-term potentiation induction. Depotentiation could also be induced at much longer times following the induction of long-term potentiation. Thus, in anaesthetized rats, depotentiation measuring 34% was induced by 10-Hz stimulation 4 h following long-term potentiation induction, and depotentiation measuring 60% was induced in two sets of experiments 24 h after long-term potentiation induction in awake animals. The results of the present study show that homosynaptic long-term depression was not induced in the adult hippocampus in vivo using stimulation protocols which are effective in hippocampal slices. However, erasure of long-term potentiation by the process of depotentiation has been shown to occur in the adult hippocampus in vivo, both at short times and at prolonged times after the induction of long-term potentiation.

摘要

在对麻醉和清醒的成年大鼠海马CA1区进行同侧Schaffer侧支/联合通路长时间低频刺激后,研究了同突触长时程抑制的诱导以及先前建立的长时程增强的去增强作用。在麻醉或清醒的成年大鼠中,1 - 10 Hz的长时间低频刺激未能诱导场兴奋性突触后电位的长时程抑制。然而,5和10 Hz(而非1或2 Hz)的长时间低频刺激确实在麻醉动物中诱导了先前建立的长时程增强的去增强作用。因此,在麻醉动物中,长时程增强诱导后10、30和40分钟给予10 Hz的900个脉冲,分别诱导了68%、59%和66%的去增强作用。在长时程增强诱导后更长时间也可诱导去增强作用。因此,在麻醉大鼠中,长时程增强诱导后4小时给予10 Hz刺激可诱导34%的去增强作用,在清醒动物的两组实验中,长时程增强诱导后24小时可诱导60%的去增强作用。本研究结果表明,在成年海马体内,使用在海马切片中有效的刺激方案不能诱导同突触长时程抑制。然而,已证明在成年海马体内,长时程增强诱导后短时间和长时间内,通过去增强过程都可消除长时程增强。

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