Evidence for Dynamic Network Regulation of Drosophila Photoreceptor Function from Mutants Lacking the Neurotransmitter Histamine.

Evidence for Dynamic Network Regulation of Drosophila Photoreceptor Function from Mutants Lacking the Neurotransmitter Histamine.
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DOI:
10.3389/fncir.2016.00019
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发表时间:
2016
影响因子:
3.5
通讯作者:
Juusola M
Juusola M
中科院分区:
医学3区
文献类型:
--
作者:
Dau A;Friederich U;Dongre S;Li X;Bollepalli MK;Hardie RC;Juusola M

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从中间神经元到光感受器的突触反馈可以通过在不断变化的光线条件下平衡视觉信息在视网膜通路上的分配来帮助优化视觉信息流。但人们对如何动态地调节这种关键的网络操作知之甚少。在这里,我们调查这个问题,通过比较野生型果蝇R1-R6光感受器的信号传导特性和性能的hdcJK 910突变体,缺乏神经递质组胺,因此不能传递信息的interneurons。记录显示,hdcJK 910光感受器从自然刺激中采集的信息量与野生型光感受器相似,但这些信息被包装在较小的响应中,特别是在明亮的照明下。分析揭示了这些改变的动力学主要是由网络过载引起的,网络过载以两种方式影响hdcJK 910光感受器。首先,丢失的抑制性组胺输入到中间神经元几乎肯定会使它们可逆地去极化,这反过来又增加了它们对hdcJK 910 R1-R6的兴奋性反馈。这种紧张性兴奋使光感受器去极化到人为的高电位,减少了它们的工作范围。第二,拯救组胺输入hdcJK 910突变体的中间神经元也恢复了正常的相位反馈调制R1-R6,导致光感受器输出加重动态强度差异在明亮的照明,类似于野生型。这些结果提供了突触反馈连接如何优化光感受器输出中的信息包装的机制解释,以及对感觉神经元动态网络调节的操作和设计的新见解。
Synaptic feedback from interneurons to photoreceptors can help to optimize visual information flow by balancing its allocation on retinal pathways under changing light conditions. But little is known about how this critical network operation is regulated dynamically. Here, we investigate this question by comparing signaling properties and performance of wild-type Drosophila R1–R6 photoreceptors to those of the hdcJK910 mutant, which lacks the neurotransmitter histamine and therefore cannot transmit information to interneurons. Recordings show that hdcJK910 photoreceptors sample similar amounts of information from naturalistic stimulation to wild-type photoreceptors, but this information is packaged in smaller responses, especially under bright illumination. Analyses reveal how these altered dynamics primarily resulted from network overload that affected hdcJK910 photoreceptors in two ways. First, the missing inhibitory histamine input to interneurons almost certainly depolarized them irrevocably, which in turn increased their excitatory feedback to hdcJK910 R1–R6s. This tonic excitation depolarized the photoreceptors to artificially high potentials, reducing their operational range. Second, rescuing histamine input to interneurons in hdcJK910 mutant also restored their normal phasic feedback modulation to R1–R6s, causing photoreceptor output to accentuate dynamic intensity differences at bright illumination, similar to the wild-type. These results provide mechanistic explanations of how synaptic feedback connections optimize information packaging in photoreceptor output and novel insight into the operation and design of dynamic network regulation of sensory neurons.