M. Rosario Sepúlveda, Frank Wuytack and Ana M. Mata High levels of Mn2+ inhibit secretory pathway Ca2+/Mn2+-ATPase (SPCA) activity and cause Golgi fragmentation in neurons and glia Journal of Neurochemistry 123
Manganese is an essential trace element, but in excess can be neurotoxic. Mn2+ overload compromises survival of neurons and glia in primary cultures specifically affecting Golgi organization. Golgi houses the Ca2+/Mn2+-ATPase SPCA, whose activity is inhibited by high Mn2+ levels. Glia is more resistant to Mn2+ toxicity than neurons and provides some protection against neurodegeneration. Furthermore, Mn2+ effects could be reversed upon Mn2+ removal.
Complete the form below and we will send an e-mail message containing a link to the selected article on your behalf