@article {48547,
	title = {Contacts between the endoplasmic reticulum and other membranes in neurons.},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	volume = {114},
	year = {2017},
	month = {2017 May 30},
	pages = {E4859-67},
	abstract = {<p>Close appositions between the membrane of the endoplasmic reticulum (ER) and other intracellular membranes have important functions in cell physiology. These include lipid homeostasis, regulation of Ca(2+) dynamics, and control of organelle biogenesis and dynamics. Although these membrane contacts have previously been observed in neurons, their distribution and abundance have not been systematically analyzed. Here, we have used focused ion beam-scanning electron microscopy to generate 3D reconstructions of intracellular organelles and their membrane appositions involving the ER (distance <=30 nm) in different neuronal compartments. ER-plasma membrane (PM) contacts were particularly abundant in cell bodies, with large, flat ER cisternae apposed to the PM, sometimes with a notably narrow lumen (thin ER). Smaller ER-PM contacts occurred throughout dendrites, axons, and in axon terminals. ER contacts with mitochondria were abundant in all compartments, with the ER often forming a network that embraced mitochondria. Small focal contacts were also observed with tubulovesicular structures, likely to be endosomes, and with sparse multivesicular bodies and lysosomes found in our reconstructions. Our study provides an anatomical reference for interpreting information about interorganelle communication in neurons emerging from functional and biochemical studies.</p>
},
	issn = {1091-6490},
	doi = {10.1073/pnas.1701078114},
	author = {Wu, Yumei and Whiteus, Christina and Xu, C Shan and Hayworth, Kenneth J and Weinberg, Richard J and Hess, Harald F and De Camilli, Pietro}
}
@article {4593,
	title = {Reduced release probability prevents vesicle depletion and transmission failure at dynamin mutant synapses.},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	volume = {109},
	year = {2012},
	month = {2012 Feb 21},
	pages = {E515-23},
	abstract = {<p>Endocytic recycling of synaptic vesicles after exocytosis is critical for nervous system function. At synapses of cultured neurons that lack the two "neuronal" dynamins, dynamin 1 and 3, smaller excitatory postsynaptic currents are observed due to an impairment of the fission reaction of endocytosis that results in an accumulation of arrested clathrin-coated pits and a greatly reduced synaptic vesicle number. Surprisingly, despite a smaller readily releasable vesicle pool and fewer docked vesicles, a strong facilitation, which correlated with lower vesicle release probability, was observed upon action potential stimulation at such synapses. Furthermore, although network activity in mutant cultures was lower, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity was unexpectedly increased, consistent with the previous report of an enhanced state of synapsin 1 phosphorylation at CaMKII-dependent sites in such neurons. These changes were partially reversed by overnight silencing of synaptic activity with tetrodotoxin, a treatment that allows progression of arrested endocytic pits to synaptic vesicles. Facilitation was also counteracted by CaMKII inhibition. These findings reveal a mechanism aimed at preventing synaptic transmission failure due to vesicle depletion when recycling vesicle traffic is backed up by a defect in dynamin-dependent endocytosis and provide new insight into the coupling between endocytosis and exocytosis.</p>
},
	issn = {1091-6490},
	doi = {10.1073/pnas.1121626109},
	author = {Lou, Xuelin and Fan, Fan and Messa, Mirko and Raimondi, Andrea and Wu, Yumei and Looger, Loren L and Ferguson, Shawn M and De Camilli, Pietro}
}
