Time course of experience-dependent synaptic potentiation and depression in barrel cortex of adolescent rats

Time course of experience-dependent synaptic potentiation and depression in barrel cortex of adolescent rats
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DOI:
10.1152/jn.1996.75.4.1714
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发表时间:
1996-04-01
影响因子:
2.5
通讯作者:
Fox, K
Fox, K
中科院分区:
医学3区
文献类型:
--
作者:
Glazewski, S;Fox, K

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1.可塑性可以诱导在(S1)桶皮质的青春期大鼠减少补充的鼻毛一侧的一个单一的胡须,为期7天,20天,或60天。剥夺的影响进行了定量评估,通过测量皮质反应刺激的备用和再生剥夺触须。用电机械刺激器产生的标准刺激诱发触须反应,用刺激后时间直方图分析法测量.发现位于II/III层的细胞在出生后28天(P28)后呈可塑性,而位于IV层的细胞则不然。对于位于D1柱周围的桶柱的II/III层的细胞,在剥夺7、20和60天后,触须优势分布显著地向备用触须移动(P <0.0001,2因素方差分析)。在任何一个剥夺时间段内,位于周围桶IV层的细胞的触须优势分布都没有显著变化(P> 0.1)。剥夺7天后,37%的细胞位于第II/III层的列剥夺触须表现出更大的反应,备用触须比他们的剥夺主触须,相比之下,11%,在正常饲养的青少年动物和3%的成年人。游离触须占优势的细胞比例在剥夺20 d后为65%,剥夺60 d后为43%.对于位于层II/III的细胞,鞘长期剥夺(7天)引起的绝对幅度的减少,响应于刺激的剥夺触须(减少到类似于28%的控制水平)。然而,没有变化可以检测到在备用(D1)触须输入相同的剥夺列。因此,D1优势度的增加主要是由于主触须反应的减少,而备用D1触须反应没有变化.第一次增加备用触须反应后,20天的剥夺。位于第II/III层的响应幅度细胞增加到70%以上的控制水平。在20天的剥夺触须刺激的反应被抑制(减少到对照的35%),这意味着在20天的触须优势转移是由于备用触须反应的增加和剥夺触须反应的减少。备用触须反应增加后60天的剥夺(110%以上的控制)在近和远的一半桶列周围D1。平均而言,被剥夺的触须反应在60天(84%的控制),虽然低于在20或7天,因为在被剥夺的桶列的远一半的反应恢复被压抑。位于离备用D1桶柱最远的桶柱的一半中的第II/III层细胞显示出正常水平的被剥夺的触须输入,而位于离备用D1桶柱最近的桶柱的一半中的细胞仍然显示出被剥夺的触须输入的降低水平(对照的54%)。对照实验表明,抑郁症的剥夺触须反应不能解释的非特异性影响。抑郁症是不是一个功能的动物的年龄,因为正常饲养的P28和成年动物表现出相似的主要触须的反应水平。这不是非特异性抑制皮质反应的结果,因为反应降低仅发生在剥夺桶柱的细胞中,而不是保留桶柱的细胞中(记录在相同的动物中)。抑郁症不是由于触须力学的改变,因为在触须被修剪而不是被去除的动物中,备用触须的反应也同样受到抑制。最后,抑郁症是输入特定的在7和20天,因为只有被剥夺的触须的反应是压抑的,而备用触须的反应要么在控制水平或在同一细胞的水平升高。Ⅱ层和Ⅱ层出现凹陷,Ⅳ层不出现凹陷。在渗透通过剥夺列,不良的反应,主要触须刺激最初遇到的第四层之前,其中响应水平是正常的,达到。在渗透通过正常列,响应水平仅略低于在surpragrantic层相比,在第四层。这表明,在剥夺7天后,可能在从IV层到II/III层的投射中,到II/III层的柱内传输被抑制。在7和20天的剥夺动物,位于最近的备用触须的桶的细胞进行了更大的减少比细胞位于中心的剥夺桶列或那些位于边缘的桶列最远的备用桶。同样,在60天的剥夺动物,在近一半的剥夺桶柱的细胞经历了更大的下降比细胞位于桶柱的远一半。一种可能的解释是,被剥夺的主触须输入的异突触抑制可能是由剩余的触须输入产生的。
1. Plasticity could be induced in (S1) barrel cortex of adolescent rats by reducing the complement of vibrissae on one side of the muzzle to a single whisker for a period of 7, 20, or 60 days. The effect of deprivation was assessed quantitatively by measuring cortical responses to stimulation of the spared and regrown deprived vibrissae. Vibrissa responses were evoked using a standard stimulus generated by an electromechanical stimulator and measured using poststimulus time histogram analysis.2. Cells located in layers II/III were found to be plastic beyond postnatal day 28 (P28), whereas cells located in layer IV were not. The vibrissa dominance distribution was shifted significantly toward the spared vibrissa after 7, 20, and 60 days of deprivation for cells located in layers II/III of barrel columns surrounding the D1 column (P < 0.0001, 2-factor analysis of variance). The vibrissa dominance distribution did not shift significantly for cells located in layer IV of surrounding barrels for any of the durations of deprivation tested (P > 0.1). After 7 days of deprivation, 37% of the cells located in layers II/III of the columns of deprived vibrissae showed greater responses to the spared vibrissae than to their deprived principal vibrissa, compared with 11% in normally reared adolescent animals and 3% in adults. The percentage of cells dominated by the spared vibrissa was 65% after 20 days of deprivation and 43% after 60 days.3. For cells located in layers II/III, shea-term deprivation (7 days) caused a decrease in the absolute magnitude of response to stimulation of the deprived vibrissa (reduction to similar to 28% of control levels). However, no change could be detected in the spared (D1) vibrissa input to the same deprived columns. Therefore the increase in D1 dominance registered in the deprived columns was mainly due to a decrease in principal vibrissa response and no change in the spared D1 vibrissa response.4. The first increase in spared vibrissa response was seen after 20 days of deprivation. The response magnitude cells located in layers II/III increased to 70% above control levels. Responses to deprived vibrissa stimulation were depressed at 20 days of depriva tion (reduction to 35% of control), implying that the vibrissa dominance shift at 20 days was due to both an increase in spared vibrissa response and a decrease in deprived vibrissa response.5. The spared vibrissa response was increased after 60 days of deprivation (110% above control) in both near and far halves of the barrel columns surrounding D1. On average, the deprived vibrissa response was depressed at 60 days (84% of control), although less than at 20 or 7 days, because of a recovery of responsiveness in the far half of the deprived barrel column. Layer II/III cells located in the half of the barrel column farthest from the spared D1 barrel column showed normal levels of deprived vibrissa input, whereas cells located in the half of the barrel column closest to the spared D1 barrel column still exhibited depressed levels of deprived vibrissa input (54% of control).6. Control experiments suggested that depression of the deprived vibrissa response could not be explained by nonspecific effects. Depression was not a function of the animal's age, because normally reared P28 and adult animals showed similar principal vibrissa response levels. It was not a result of nonspecific depression of cortical responses, because the decreased response only occurred in cells of deprived barrel columns and not spared barrel columns (recorded in the same animals). Depression was not due to altered vibrissa mechanics, because the spared vibrissa response was similarly depressed in animals in which the vibrissae had been trimmed rather than removed. Finally, depression was input specific at 7 and 20 days, because only the deprived vibrissa responses were depressed, whereas spared vibrissa responses were either at control levels or at elevated levels for the same cells.7. Depression occurred in layers II and In, but not in layer IV. In penetrations down through deprived columns, poor responses to principal vibrissa stimulation were encountered initially before layer IV, where response levels were normal, was reached. In penetrations down through normal columns, response levels were only marginally less in surpragranular layers compared with those in layer IV. This suggests that intracolumnar transmission to layers II/III is depressed after 7 days of deprivation, possibly in the projection from layer IV to layers II/III.8. In 7- and 20-day deprived animals, the cells located nearest to the spared vibrissa's barrel underwent a greater decrease in response than did cells located in the center of the deprived barrel column or those located at the edge of the barrel column farthest from the spared barrel. Similarly, in 60-day deprived animals, cells in the near half of the deprived barrel column underwent a greater decrease in response than did cells located in the far half of the barrel column. One possible explanation is that a heterosynaptic depression of the deprived principal vibrissa input may be produced by the spared vibrissa input.