Activity-driven sharpening of the retinotectal projection in goldfish: development under stroboscopic illumination prevents sharpening.

Activity-driven sharpening of the retinotectal projection in goldfish: development under stroboscopic illumination prevents sharpening.
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金鱼视网膜顶盖投影的活动驱动锐化:频闪照明下的发育可防止锐化。

DOI:
10.1002/neu.480240310
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发表时间:
1993
期刊:
Journal of neurobiology
影响因子:
--
通讯作者:
Buzzard,M
Buzzard,M
中科院分区:
--
文献类型:
--
作者:
Schmidt,JT;Buzzard,M

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在视网膜顶盖投影再生过程中,阻断或同步活动可阻止记录在顶盖上的视网膜定位图的锐化和图平面内单个乔木结构的细化,而这种细化是由n -甲基- d -天冬氨酸(NMDA)受体触发的。我们测试了活动驱动的细化是否也发生在幼体和成年金鱼的投射发育过程中。孵化后不久,金鱼幼鱼被放置在一个密闭的箱中,由氙气频闪灯以1hz的频率照明,每天循环14小时。鱼被饲养1.5-2年,直到大到足以在我们的视顶板测绘仪(6厘米长)中记录。年龄和大小匹配的对照有法线图,在每个顶点记录的多单元感受野(murf)为10.8°(0.16 S.E.M,n= 5),而频栅饲养的鱼只有大致的视网膜主题图,murf大大扩大,平均为26.7°(1.41 S.E.M,n= 5)。这种扩大表示在每个顶点上的异常收敛,因为地图在开发过程中未能锐化。用辣根过氧化物酶(HRP)对幼鱼和成年对照鱼的视网膜轴突进行染色。用透视相机在全顶坐骑上绘制,分析其在视网膜定位图平面上的空间范围、分支顺序、分支末端数量、终止深度和母轴突口径。幼鱼(1 ~ 2周龄)的乔木体积小(约50 × 40 μm),分枝数小于10个,属单一层,不能按轴突直径划分为不同的类。对照成鱼(6 cm长)染色的87根木条与之前检测的成鱼非常相似,细轴突、中轴突和粗轴突的平均长度分别为115、166和194 μm,有17-24个分枝末梢。12条频闪养殖鱼的110个分枝常出现异常。虽然束状运动正常,但束外运动路径异常,呈反转状。轴突通常沿着它们的路线有分支,这些分支分散在更大的范围内,而不是形成一个明显的簇。相比之下,任何组的分支数量和终止深度都没有明显变化。粗口径的乔木异常最多,比对照长64%,宽30%。细径乔木也显著增大了约20%,而中径乔木没有增大。增大的乔木部分解释了未锐化的电生理图。综上所述,研究结果表明,在发育和再生过程中,视网膜顶图受到活动驱动的锐化过程的影响。©1993 John Wiley & Sons, Inc
Blocking or synchronizing activity during regeneration of the retinotectal projection prevents both the sharpening of the retinotopic map recorded on tectum and the refinement of the structure of individual arbors within the plane of the map, and this refinement is triggered byN‐methyl‐d‐aspartate (NMDA) receptors. We tested whether activity‐driven refinement also occurs during development of the projection in larval and young adult goldfish. Shortly after hatching, larval goldfish were placed into tanks within light‐tight chambers illuminated by a xenon strobe at 1 Hz for 14 h of each daily cycle. Fish were reared for 1.5–2 years, until large enough to record in our retinotectal mapping apparatus (6 cm length). Age‐ and size‐matched controls had normal maps with multiunit receptive fields (MURFs) recorded at each tectal point of 10.8° (0.16 S.E.M.,n= 5), whereas the strobe‐reared fish had only roughly retino‐topic maps with much enlarged MURFs averaging 26.7° (1.41 S.E.M.,n= 5). This enlargement represents an abnormal convergence onto each tectal point, as the maps failed to sharpen during development. The arbors of individual retinal axons were stained with horseradish peroxidase (HRP) in larval fish and in adult strobereared and control fish. They were drawn with camera lucida from tectal whole mounts, and analyzed for spatial extent in the plane of the retinotopic map, order of branching, number of branch endings, depth of termination, and caliber of the parent axon. Arbors from larval fish (1–2 weeks) were small (approximately 50 × 40 μm) with less than 10 branches, occupied a single strata, and could not be separated into different classes by caliber of axon. The 87 arbors stained in control adult fish (6 cm long) were much like previously examined adult arbors, with those from fine, medium, and coarse axons averaging 115, 166, and 194 μm in extent, respectively, and having 17–24 branch endings. The 110 arbors from 12 strobe‐reared fish were often abnormal. Although the fasciculation was normal, the extrafascicular routes were abnormal with reversing turns. The axons often had branches along their course, and these branches were scattered across a wider extent, rather than forming a distinct cluster. In contrast, neither the number of branches nor the depths of termination was significantly changed in any group. The coarse caliber arbors were most abnormal, being 64% longer and 30% wider than controls. The fine caliber arbors were also significantly larger by about 20%, but the medium caliber arbors were not enlarged. The enlarged arbors partially account for the unsharpened electrophysiological maps. Together the results show that during development, as well as during regeneration, the retinotectal map is subject to an activity‐driven sharpening process. © 1993 John Wiley & Sons, Inc.
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DOI: --
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