Adenosine 5′-Triphosphate (ATP) Inhibits Schwann Cell Demyelination During Wallerian Degeneration

• Published in: Cellular and molecular neurobiology 2014-04, Vol.34 (3), p.361-368
• Main Authors: Shin, Youn Ho, Chung, Hyung-Joo, Park, Chan, Jung, Junyang, Jeong, Na Young
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - pharmacology; Adenosine Triphosphate - therapeutic use; Animals; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cells, Cultured; Demyelinating Diseases - pathology; Demyelinating Diseases - prevention & control; Male; Mice; Mice, Inbred C57BL; Neurobiology; Neurosciences; Organ Culture Techniques; Original Research; Schwann Cells - drug effects; Schwann Cells - pathology; Wallerian Degeneration - drug therapy; Wallerian Degeneration - pathology
• ISSN: 0272-4340; 1573-6830; 1573-6830
• DOI: 10.1007/s10571-013-0020-y

Adenosine 5′-triphosphate (ATP) is implicated in intercellular communication as a neurotransmitter in the peripheral nervous system. In addition, ATP is known as lysosomal exocytosis activator. In this study, we investigated the role of extracellular ATP on demyelination during Wallerian degeneration (WD) using ex vivo and in vivo nerve degeneration models. We found that extracellular ATP inhibited myelin fragmentation and axonal degradation during WD. Furthermore, metformin and chlorpromazine, lysosomal exocytosis antagonists blocked the effect of ATP on the inhibition of demyelination. Thus, these findings indicate that ATP-induced-lysosomal exocytosis may be involved in demyelination during WD.