Smear Matthew C, Tao Huizhong W, Staub Wendy, Orger Michael B, Gosse Nathan J, Liu Yan, Takahashi Koji, Poo Mu-Ming, Baier Herwig
University of California, San Francisco, Department of Physiology, Program in Neuroscience, 1550 4th Street, San Francisco, CA 94143, USA.
Neuron. 2007 Jan 4;53(1):65-77. doi: 10.1016/j.neuron.2006.12.013.
The neural circuitry that constrains visual acuity in the CNS has not been experimentally identified. We show here that zebrafish blumenkohl (blu) mutants are impaired in resolving rapid movements and fine spatial detail. The blu gene encodes a vesicular glutamate transporter expressed by retinal ganglion cells. Mutant retinotectal synapses release less glutamate, per vesicle and per terminal, and fatigue more quickly than wild-type in response to high-frequency stimulation. In addition, mutant axons arborize more extensively, thus increasing the number of synaptic terminals and effectively normalizing the combined input to postsynaptic cells in the tectum. This presumably homeostatic response results in larger receptive fields of tectal cells and a degradation of the retinotopic map. As predicted, mutants have a selective deficit in the capture of small prey objects, a behavior dependent on the tectum. Our studies successfully link the disruption of a synaptic protein to complex changes in neural circuitry and behavior.
中枢神经系统中限制视敏度的神经回路尚未通过实验确定。我们在此表明，斑马鱼blumenkohl（blu）突变体在分辨快速运动和精细空间细节方面存在缺陷。blu基因编码一种由视网膜神经节细胞表达的囊泡谷氨酸转运体。与野生型相比，突变体视网膜 - 脑顶盖突触每个囊泡和每个终末释放的谷氨酸较少，并且在高频刺激下比野生型更快疲劳。此外，突变体轴突的分支更广泛，从而增加了突触终末的数量，并有效地使脑顶盖中突触后细胞的综合输入正常化。这种推测的稳态反应导致脑顶盖细胞的感受野更大，以及视网膜拓扑图的退化。正如所预测的，突变体在捕获小猎物对象方面存在选择性缺陷，这是一种依赖于脑顶盖的行为。我们的研究成功地将一种突触蛋白的破坏与神经回路和行为的复杂变化联系起来。
