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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Low-frequency stimulation induces homosynaptic depotentiation but not long-term depression of synaptic transmission in the adult anaesthetized and awake rat hippocampus in vivo.
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Low-frequency stimulation induces homosynaptic depotentiation but not long-term depression of synaptic transmission in the adult anaesthetized and awake rat hippocampus in vivo.

机译:低频刺激在体内麻醉和清醒的成年大鼠海马中诱导了突触的去势,但不会长期抑制突触传递。

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摘要

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.
机译:在长期同侧低频刺激Schaffer侧支/连合通路后,在麻醉和清醒的成年大鼠的CA1海马区中研究了先前建立的长期增强的同突触长期抑制和去势。在麻醉或清醒的成年大鼠中,长期以1-10 Hz的低频刺激未能引起长期的场兴奋性突触后突触电位抑制。然而,尽管不是在1或2 Hz的频率下,在5和10 Hz的低频刺激时间延长,却确实导致了麻醉动物先前建立的长期增强作用的减弱。因此,在麻醉动物中,在长期增强诱导后10、30和40分钟给予900Hz,10Hz的脉冲诱导68。%,59%和66%的去势。诱导长时程增强后,去长效也可以诱导更长的时间。因此,在麻醉的大鼠中,长期增强诱导后4 h,通过10 Hz刺激诱导了34%的去势化,而在长期增强诱导后24 h的两组实验中,在两组实验中诱导了60%的去势化。本研究的结果表明,使用对海马片有效的刺激方案,在体内成人海马中不诱发同突触长期抑制。然而,已经证明在成人长期海马体内,通过去势化作用消除长期增强作用在诱导长期增强作用后的短时间内和长时间内都存在。

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