Wenhui Zhong, Zhongqun Chen, Shaoxuan Wang, Jun Cao, Xin Lin, Xiaoqian Lai, Bilin Rao, Jun Zhang
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引用次数: 0
Abstract
The synuclein family comprises three presynaptic proteins-alpha-synuclein (α-Syn), beta-synuclein (β-Syn), and gamma-synuclein (γ-Syn)-which are crucial for synaptic transmission. Our previous studies have detailed the precise cellular and subcellular localization of α- and β-Syn in the adult mouse retina, revealing distinct expression patterns in excitatory and inhibitory synaptic elements. The balance between excitatory and inhibitory neurotransmitters in the inner plexiform layer (IPL) is critical for neural development in the mouse retina. Here, we employed light-microscopic immunocytochemistry to investigate the expression of α- and β-Syn in the developing mouse retina, examining from embryonic day 13.5 to postnatal day 21 (E13.5, E16.5, E19.5, P1, P7, P10, P14, and P21). We revealed distinct developmental expression patterns across these stages. We found that α-Syn was first detected at E13.5, whereas β-Syn expression appeared later at E16.5. After E16.5, β-Syn exhibited a broader expression profile compared to α-Syn. Consistent with findings in the adult retina, α-Syn was confined to inhibitory synapses, while β-Syn was present in both excitatory and inhibitory synapses during development. These unique expression patterns of α- and β-Syn in the developing retina suggest potential roles in modulating excitatory and inhibitory inputs during retinal maturation. Furthermore, this research may contribute to understanding the broader role of α- and β-Syn in neural development within the central nervous system.
期刊介绍:
Brain Structure & Function publishes research that provides insight into brain structure−function relationships. Studies published here integrate data spanning from molecular, cellular, developmental, and systems architecture to the neuroanatomy of behavior and cognitive functions. Manuscripts with focus on the spinal cord or the peripheral nervous system are not accepted for publication. Manuscripts with focus on diseases, animal models of diseases, or disease-related mechanisms are only considered for publication, if the findings provide novel insight into the organization and mechanisms of normal brain structure and function.