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大鼠运动皮层水平连接的长期抑制

Long-term depression of horizontal connections in rat motor cortex.

作者信息

Hess G, Donoghue J P

机构信息

Department of Animal Physiology, Institute of Zoology, Jagiellonian University, Krakow, Poland.

出版信息

Eur J Neurosci. 1996 Apr;8(4):658-65. doi: 10.1111/j.1460-9568.1996.tb01251.x.

Abstract

The possibility for long-term depression (LTD) of synaptic transmission in layer II/III horizontal connections within motor cortex was investigated using field potentials and intracellular recordings in rat brain slices. The LTD was induced by low-frequency stimulation at 2 Hz for 10 min in sites displaced horizontally by 0.5 mm from the stimulating electrode. Response amplitude measured 25-30 min after 2 Hz stimulation ended was 79% of baseline values (n = 13) at half maximal stimulation and 59% when 2 Hz stimulus intensity was doubled (n = 10). In 13/15 tested cases LTD in horizontal connections was specific to the activated pathway. Intracellular recordings from six neurons confirmed synaptic character of response depression. Horizontal connections in which LTD was induced retained the capability of increasing synaptic strength. Long-term potentiation could be induced in previously depressed pathways by simultaneous theta burst stimulation of two converging horizontal inputs combined with transient local application of GABA(A) receptor antagonist bicuculline methiodide (mean increase: 45 +/- 8% n = 6) or by simultaneous theta burst stimulation of converging horizontal and vertical inputs (mean change: 26 +/- 6%, n = 5). These data demonstrate that activity-dependent mechanisms may regulate bidirectionally the effectiveness of horizontal synaptic coupling between cortical neurons, thus forming a potential mechanism for plasticity of cortical connections and the representation patterns they support.

摘要

利用大鼠脑片的场电位和细胞内记录,研究了运动皮层II/III层水平连接中突触传递长时程抑制(LTD)的可能性。LTD通过在距刺激电极水平位移0.5 mm处进行2 Hz的低频刺激10分钟来诱导。在2 Hz刺激结束后25 - 30分钟测量的反应幅度,在半最大刺激时为基线值的79%(n = 13),当2 Hz刺激强度加倍时为59%(n = 10)。在15个测试案例中的13个,水平连接中的LTD对激活的通路具有特异性。来自六个神经元的细胞内记录证实了反应抑制的突触特性。诱导出LTD的水平连接保留了增加突触强度的能力。通过同时对两个汇聚的水平输入进行θ爆发刺激并短暂局部应用GABA(A)受体拮抗剂甲硫双氢麦角碱(平均增加:45 +/- 8%,n = 6),或通过同时对汇聚的水平和垂直输入进行θ爆发刺激(平均变化:26 +/- 6%,n = 5),可以在先前抑制的通路中诱导长时程增强。这些数据表明,活动依赖机制可能双向调节皮层神经元之间水平突触耦合的有效性,从而形成皮层连接可塑性及其支持的表征模式的潜在机制。

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