Answers are grounded in this paper and cite their sources.
Experimental study reveals glia-derived cholesterol promotes synapse maturation in central nervous system neurons, indicating that cholesterol availability limits synaptogenesis.
The molecular mechanisms controlling synaptogenesis in the central nervous system (CNS) are poorly understood. Previous reports showed that a glia-derived factor strongly promotes synapse development in cultures of purified CNS neurons. Here, we identify this factor as cholesterol complexed to apolipoprotein E-containing lipoproteins. CNS neurons produce enough cholesterol to survive and grow, but the formation of numerous mature synapses demands additional amounts that must be provided by glia. Thus, the availability of cholesterol appears to limit synapse development. This may explain the delayed onset of CNS synaptogenesis after glia differentiation and neurobehavioral manifestations of defects in cholesterol or lipoprotein homeostasis.
No takes yet. Share an insight, caveat, or question.
Mauch et al. (2001) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: