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Updated: Jul 27, 2026
Patch Clamp Recording of Starburst Amacrine Cells in a Flat-mount Preparation of Deafferentated Mouse Retina
Published on: October 13, 2016
Changes in Starburst Amacrine Cells in Mice with Diabetic Retinopathy
Jae-Rim Son1, Myung-Jun Lee1,2, Chang-Jin Jeon1,2,3
1Department of Biology, School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, 41566 Daegu, Republic of Korea.
Background:
Neurodegenerative diseases, such as diabetic retinopathy (DR) and glaucoma, induce retinal neuron loss. Acetylcholine-containing cholinergic neurons, known as starburst amacrine cells (SACs), play critical roles in the generation of precise neuronal activity in the retina and are located in the inner nuclear layer (INL, conventional) and ganglion cell layer (GCL, displaced).
Methods:
This study investigated the loss of and morphological changes in SACs in the retinas of streptozotocin (STZ)-induced diabetic and insulin-deficient C57BL/6-Tg(pH1-siRNAinsulin/CMV-hIDE)/Korl (IDCK) mice. SACs were immunocytochemically localized with anti-choline acetyltransferase (ChAT) antibody, and ChAT-labeled cells in the INL and GCL in the control and experimental groups were counted along the central vertical meridian in the whole-mounted retina using conventional fluorescent or confocal microscopes.
Results:
ChAT-immunoreactive (IR) neurons in STZ-induced diabetic mouse retina decreased by 8.34% at 4-6 weeks and by 14.89% at 42 weeks compared with the control group. Localized ChAT-IR neuron counts in the retinas of 20-week-old IDCK mice were 16.80% lower than those of age-matched control mice. Cell body deformation and aggregation were detected in the retinas of mice with DR. Single-cell injection experiments revealed the loss and deformation of dendritic branches in ChAT-IR neurons in DR. All ChAT-IR neurons expressed the calcium-binding protein calretinin, whereas no ChAT-IR neuron colocalized with calbindin-D28K or parvalbumin.
Conclusions:
Our results revealed that the neurodegenerative effects of the loss and deformation of ChAT-IR neurons can provide a reference for future study of this disease.
