Mechanisms of retinal information processing during eye movements

2022 Fiscal Year Final Research Report

• Project/Area Number: 19K06915
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 46010:Neuroscience-general-related
• Research Institution: Ritsumeikan University
• Principal Investigator: Tachibana Masao 立命館大学, 総合科学技術研究機構, 教授 (60132734)
• Co-Investigator(Kenkyū-buntansha): 小池 千恵子 立命館大学, 薬学部, 教授 (80342723)
• Project Period (FY): 2019-04-01 – 2023-03-31
• Keywords: 網膜 / 網膜神経節細胞 / 受容野 / 眼球運動 / 周期的発火

Outline of Final Research Achievements

We investigated whether the visual information processing mechanism of the retina changes depending on the internal and external environment. After injecting a tracer into the superior colliculus of mice, retinal ganglion cells were retrogradely fluorescent labeled, and morphologically classified into 24 subtypes. We examined electrophysiologically the response characteristics of retinal ganglion cells to video stimuli mimicking eye movements, and found that the receptive field properties were changed in both goldfish and mouse retinae.
Deletion of TRPM1 channel expressed in ON-type bipolar cells caused only a subtle change in the retinal structure, but retinal ganglion cells showed abnormal periodic firing, which was induced not by themselves but by periodic synaptic input. Although deletion of a gene involved in cell adhesion in the outer limiting membrane caused a disorder of the photoreceptor layer, retinal ganglion cells exhibited similar abnormal periodic firing.

Free Research Field

視覚神経科学

Academic Significance and Societal Importance of the Research Achievements

網膜のON型双極細胞に発現するTRPM1チャネルを欠損させると、網膜構造にほとんど変化がないにも関わらず、網膜神経節細胞は異常な周期的発火を示した。一方、外境界膜の細胞接着関連遺伝子を欠損させると構造異常はほぼ視細胞層に限局していたが、網膜神経節細胞に類似した異常な周期的発火が認められた。このように、網膜に発現する遺伝子を欠損させると、層構造の変化に程度の差異があっても、網膜回路ダイナミクスが変化して周期的発火を生じることが示唆された。網膜疾患患者における光視症等の原因探索の手がかりになると期待できる。