Odd-petal states and persistent flows in spin-orbit-coupled Bose-Einstein condensates

We study the phase diagram of a Rashba spin-orbit-coupled Bose-Einstein condensate confined in a two-dimensional toroidal trap. In the immiscible regime we find an azimuthally periodic density distribution, with the periodicity highly tuneable as a function of the spin-orbit coupling strength and which favours an odd number of petals in each component. This allows for a wide range of states that can be created. We further show that in the miscible regime, both components possess states with persistent flows with a unit winding number difference between them and with the absolute values of these winding numbers depending on the spin-orbit coupling strength. All features of the odd-petal and the persistent flow states can be explained using a simple but effective model.Comment: 5 pages, 2 figure

Inactivation of presenilins causes pre-synaptic impairment prior to post-synaptic dysfunction

Synaptic dysfunction is widely thought to be a pathogenic precursor to neurodegeneration in Alzheimer’s disease (AD), and the extent of synaptic loss provides the best correlate for the severity of dementia in AD patients. Presenilins 1 and 2 are the major causative genes of early‐onset familial AD. Conditional inactivation of presenilins in the adult cerebral cortex results in synaptic dysfunction and memory impairment, followed by age‐dependent neurodegeneration. To characterize further the consequence of presenilin inactivation in the synapse, we evaluated the temporal development of pre‐synaptic and post‐synaptic deficits in the Schaeffer‐collateral pathway of presenilin conditional double knockout (PS cDKO) mice prior to onset of neurodegeneration. Following presenilin inactivation at 4 weeks, synaptic facilitation and probability of neurotransmitter release are impaired in PS cDKO mice at 5 weeks of age, whereas post‐synaptic NMDA receptor (NMDAR)‐mediated responses are normal at 5 weeks but impaired at 6 weeks of age. Long‐term potentiation induced by theta burst stimulation is also reduced in PS cDKO mice at 6 weeks of age. These results show that loss of presenilins results in pre‐synaptic deficits in short‐term plasticity and probability of neurotransmitter release prior to post‐synaptic NMDAR dysfunction, raising the possibility that presenilins may regulate post‐synaptic NMDAR function in part via a trans‐synaptic mechanism.This work was supported by the National Institute of Health NS041783 (to J.S.). We would like to thank Xiaoyan Zou and Huailong Zhao for technical assistance. (NS041783 - National Institute of Health)Published versio