Dislocations and vortices in pair density wave superconductors

With the ground breaking work of the Fulde, Ferell, Larkin, and Ovchinnikov (FFLO), it was realized that superconducting order can also break translational invariance; leading to a phase in which the Cooper pairs develop a coherent periodic spatially oscillating structure. Such pair density wave (PDW) superconductivity has become relevant in a diverse range of systems, including cuprates, organic superconductors, heavy fermion superconductors, cold atoms, and high density quark matter. Here we show that, in addition to charge density wave (CDW) order, there are PDW ground states that induce spin density wave (SDW) order when there is no applied magnetic field. Furthermore, we show that PDW phases support topological defects that combine dislocations in the induced CDW/SDW order with a fractional vortex in the usual superconducting order. These defects provide a mechanism for fluctuation driven non-superconducting CDW/SDW phases and conventional vortices with CDW/SDW order in the core.Comment: 6 pages,1 figure, 1 tabl

A Bcl-xL–Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis

Following exocytosis, the rate of recovery of neurotransmitter release is determined by vesicle retrieval from the plasma membrane and by recruitment of vesicles from reserve pools within the synapse, the latter of which is dependent on mitochondrial ATP. The Bcl-2 family protein Bcl-x(L), in addition to its role in cell death, regulates neurotransmitter release and recovery in part by increasing ATP availability from mitochondria. We now find, however, that, Bcl-x(L) directly regulates endocytotic vesicle retrieval in hippocampal neurons through protein/protein interaction with components of the clathrin complex. Our evidence suggests that, during synaptic stimulation, Bcl-x(L) translocates to clathrin-coated pits in a calmodulin-dependent manner and forms a complex of proteins with the GTPase Drp1, Mff and clathrin. Depletion of Drp1 produces misformed endocytotic vesicles. Mutagenesis studies suggest that formation of the Bcl-x(L)-Drp1 complex is necessary for the enhanced rate of vesicle endocytosis produced by Bcl-x(L), thus providing a mechanism for presynaptic plasticity