Coupling a single electron to a Bose-Einstein condensate

The coupling of electrons to matter is at the heart of our understanding of material properties such as electrical conductivity. One of the most intriguing effects is that electron-phonon coupling can lead to the formation of a Cooper pair out of two repelling electrons, the basis for BCS superconductivity. Here we study the interaction of a single localized electron with a Bose-Einstein condensate (BEC) and show that it can excite phonons and eventually set the whole condensate into a collective oscillation. We find that the coupling is surprisingly strong as compared to ionic impurities due to the more favorable mass ratio. The electron is held in place by a single charged ionic core forming a Rydberg bound state. This Rydberg electron is described by a wavefunction extending to a size comparable to the dimensions of the BEC, namely up to 8 micrometers. In such a state, corresponding to a principal quantum number of n=202, the Rydberg electron is interacting with several tens of thousands of condensed atoms contained within its orbit. We observe surprisingly long lifetimes and finite size effects due to the electron exploring the wings of the BEC. Based on our results we anticipate future experiments on electron wavefunction imaging, investigation of phonon mediated coupling of single electrons, and applications in quantum optics.Comment: 4 pages, 3 figures and supplementary informatio

Quantum critical behavior in strongly interacting Rydberg gases

We study the appearance of correlated many-body phenomena in an ensemble of atoms driven resonantly into a strongly interacting Rydberg state. The ground state of the Hamiltonian describing the driven system exhibits a second order quantum phase transition. We derive the critical theory for the quantum phase transition and show that it describes the properties of the driven Rydberg system in the saturated regime. We find that the suppression of Rydberg excitations known as blockade phenomena exhibits an algebraic scaling law with a universal exponent.Comment: 4 pages, 3 figures, published versio

An experimental and theoretical guide to strongly interacting Rydberg gases

We review experimental and theoretical tools to excite, study and understand strongly interacting Rydberg gases. The focus lies on the excitation of dense ultracold atomic samples close to, or within quantum degeneracy, to high lying Rydberg states. The major part is dedicated to highly excited S-states of Rubidium, which feature an isotropic van-der-Waals potential. Nevertheless, the setup and the methods presented are also applicable to other atomic species used in the field of laser cooling and atom trapping.Comment: 23 pages, 22 figures, tutoria

Quantum critical behavior in strongly interacting Rydberg gases

We study the appearance of correlated many-body phenomena in an ensemble of atoms driven resonantly into a strongly interacting Rydberg state. The ground state of the Hamiltonian describing the driven system exhibits a second order quantum phase transition. We derive the critical theory for the quantum phase transition and show that it describes the properties of the driven Rydberg system in the saturated regime. We find that the suppression of Rydberg excitations known as blockade phenomena exhibits an algebraic scaling law with a universal exponent.Comment: 4 pages, 3 figures, published versio

Locomotor deficits in a mouse model of ALS are paralleled by loss of V1-interneuron connections onto fast motor neurons

Funding: This work was supported by the Lundbeck Foundation (I.A.), the Björklund foundation (I.A.), the A.P. Møller foundation (I.A.), the Novo Nordisk Laureate Program (O.K., NNF15OC0014186), The Lundbeck Foundation (O.K.), the Louis-Hansen foundation (R.M.R.) and The Faculty of Health and Medical Sciences (O.K.).ALS is characterized by progressive inability to execute movements. Motor neurons innervating fast-twitch muscle-fibers preferentially degenerate. The reason for this differential vulnerability and its consequences on motor output is not known. Here, we uncover that fast motor neurons receive stronger inhibitory synaptic inputs than slow motor neurons, and disease progression in the SOD1G93A mouse model leads to specific loss of inhibitory synapses onto fast motor neurons. Inhibitory V1 interneurons show similar innervation pattern and loss of synapses. Moreover, from postnatal day 63, there is a loss of V1 interneurons in the SOD1G93A mouse. The V1 interneuron degeneration appears before motor neuron death and is paralleled by the development of a specific locomotor deficit affecting speed and limb coordination. This distinct ALS-induced locomotor deficit is phenocopied in wild-type mice but not in SOD1G93A mice after appearing of the locomotor phenotype when V1 spinal interneurons are silenced. Our study identifies a potential source of non-autonomous motor neuronal vulnerability in ALS and links ALS-induced changes in locomotor phenotype to inhibitory V1-interneurons.Publisher PDFPeer reviewe

Colocalization of synapsin and actin during synaptic vesicle recycling

It has been hypothesized that in the mature nerve terminal, interactions between synapsin and actin regulate the clustering of synaptic vesicles and the availability of vesicles for release during synaptic activity. Here, we have used immunogold electron microscopy to examine the subcellular localization of actin and synapsin in the giant synapse in lamprey at different states of synaptic activity. In agreement with earlier observations, in synapses at rest, synapsin immunoreactivity was preferentially localized to a portion of the vesicle cluster distal to the active zone. During synaptic activity, however, synapsin was detected in the pool of vesicles proximal to the active zone. In addition, actin and synapsin were found colocalized in a dynamic filamentous cytomatrix at the sites of synaptic vesicle recycling, endocytic zones. Synapsin immunolabeling was not associated with clathrin-coated intermediates but was found on vesicles that appeared to be recycling back to the cluster. Disruption of synapsin function by microinjection of antisynapsin antibodies resulted in a prominent reduction of the cytomatrix at endocytic zones of active synapses. Our data suggest that in addition to its known function in clustering of vesicles in the reserve pool, synapsin migrates from the synaptic vesicle cluster and participates in the organization of the actin-rich cytomatrix in the endocytic zone during synaptic activity