Tetraspanin2 (Tspan2) is a member of the tetraspan/transmembrane4 superfamily restricted to the nervous system. The abundance of Tspan2 is low in physiological condition but increases greatly in myelin of PLP-deficient mice which may indicate its’ compensatory functions. Our experiments show that Tspan2 has no effect on delay of myelination at P14; young and old mice lacking Tspan2 has the same g-ratio as wild type. However, the quantity of unhealthy axons and axonal swellings are higher in aged animals lacking both PLP and Tspan2 than in single PLP knockout. Furthermore,the absence of PLP causes the decrease in the number of axons and rise in axon diameter; lack of
Tspan2 alone leads to decrease in quantity of 0.4-0.7 µm diameter axons in 40 weeks old mice. These findings point to a possible auxiliary role of Tspan2 in support of axonal transport and long-term axon preservation in PLP null condition.
Inhaltsverzeichnis (Table of Contents)
- ABSTRACT
- INTRODUCTION
- MATERIALS AND METHODS
- Animals
- Electron and light microscopy
- Morphometric analysis of electron micrographs
- Quantification of myelinated vs. nonmyelinated axons
- Validation of axon pathologies
- g-ratio and axon diameter
Zielsetzung und Themenschwerpunkte (Objectives and Key Themes)
This study investigates the potential compensatory role of tetraspanin 2 (Tspan2) in the absence of proteolipid protein (PLP), a crucial component of myelin sheaths. The research aims to determine if Tspan2 can mitigate the delay of myelination and/or the degeneration of axons in PLP-deficient mice.- The role of Tspan2 in myelin formation and axonal health in the absence of PLP
- The impact of Tspan2 deficiency on axonal degeneration in PLP-deficient mice
- The potential compensatory mechanisms of Tspan2 for PLP functions
- The relationship between Tspan2 and axonal transport and preservation
- The significance of Tspan2 in the context of myelination and neuroprotection
Zusammenfassung der Kapitel (Chapter Summaries)
- ABSTRACT: This section provides a concise overview of the research, highlighting the potential compensatory role of Tspan2 in PLP-deficient mice. It summarizes the key findings, suggesting that Tspan2 may contribute to axonal transport and long-term preservation in the absence of PLP.
- INTRODUCTION: This chapter introduces the concept of myelination and its importance in the nervous system. It discusses the role of myelin in electrical insulation, axonal transport, and the implications of demyelination. The chapter also presents the significance of proteolipid protein (PLP) in myelin formation and the potential compensatory mechanisms that arise in its absence.
- MATERIALS AND METHODS: This section details the experimental design and procedures, outlining the animal models used, the microscopy techniques employed, and the morphometric analyses performed. The methodology allows for the quantification of myelinated and nonmyelinated axons, assessment of axonal pathologies, and the determination of g-ratios and axonal diameters.
Schlüsselwörter (Keywords)
The central keywords of this study are: myelin, proteolipid protein (PLP), tetraspanin 2 (Tspan2), axonal degeneration, myelination, neuroprotection, axonal transport, and compensatory mechanisms. The study focuses on the relationship between these elements and the potential role of Tspan2 in mitigating the effects of PLP deficiency on the nervous system.- Arbeit zitieren
- Maryna Psol (Autor:in), 2012, Tetraspanin2 is a candidate for compensation of PLP functions, München, GRIN Verlag, https://www.hausarbeiten.de/document/233026
