Observation of Quantum Shock Waves Created with Ultra Compressed Slow Light Pulses in a Bose-Einstein Condensate

We have used an extension of our slow light technique to provide a method for inducing small density defects in a Bose-Einstein condensate. These sub-resolution, micron-sized defects evolve into large amplitude sound waves. We present an experimental observation and theoretical investigation of the resulting breakdown of superfluidity. We observe directly the decay of the narrow density defects into solitons, the onset of the `snake' instability, and the subsequent nucleation of vortices.Comment: 15 pages, 5 figure

A High Flux Source of Cold Rubidium

We report the production of a continuous, slow, and cold beam of 87-Rb atoms with an unprecedented flux of 3.2 x 10^12 atoms/s and a temperature of a few milliKelvin. Hot atoms are emitted from a Rb candlestick atomic beam source and transversely cooled and collimated by a 20 cm long atomic collimator section, augmenting overall beam flux by a factor of 50. The atomic beam is then decelerated and longitudinally cooled by Zeeman slowing

Ultraslow Light & Bose-Einstein Condensates: Two-way Control with Coherent Light & Atom Fields

Ultraslow light has been used to form dramatic new nonlinear excitations in superfluid Bose-Einstein condensates of laser-cooled alkali atoms, and to create pulsed coherent matter waves. We describe these phenomena and a novel single-atom detector for use in studying the waves' coherence properties.Engineering and Applied SciencesPhysic

Cellular actions of opioids on periaqueductal grey neurons from C57B16/J mice and mutant mice lacking MOR-1

1. Patch clamp recordings were made from periaqueductal grey (PAG) neurons in vitro to investigate the cellular actions of opioids in wild-type C57B16/J mice and mutant mice lacking the first exon of the μ-opioid (MOP) receptor. 2. In wild-type mice, the κ-(KOP) agonist U-69593 (300 nM) and the mixed μ/δ-opioid agonist met-enkephalin (10 μM), but not the δ-(DOP) agonist deltorphin (300 nM), reduced the amplitude of evoked GABA(A)-mediated inhibitory postsynaptic currents (IPSCs). Met-enkephalin and U-69593 also reduced the rate of spontaneous miniature IPSCs, but had no effect on their amplitude and kinetics. In μ-receptor-deleted mice, only U-69593 (300 nM) reduced the amplitude of evoked IPSCs. 3. In wild-type mice, the MOP agonist DAMGO (3 μM) produced an outward current in 76% of the neurons. Deltorphin and U-69593 produced outward currents in 24 and 32% of the neurons, respectively. In μ-receptor-deleted mice, deltorphin and U-69593 produced similar outward currents in 32 and 27% of the neurons, respectively, while DAMGO was without effect. All neurons in both the wild-type and μ-receptor-deleted mice responded with similar outward currents to either the GABA(B) receptor agonist baclofen (10 μM), or the opioid-like receptor ORL1 (NOP) agonist nociceptin (300 nM). 4. The DAMGO-, deltorphin-, U-69593-, baclofen- and nociceptin-induced currents displayed inward rectification and reversed polarity at −109 to −116 mV. 5. These findings indicate that μ-, δ- and κ-opioid receptor activation has complex pre- and postsynaptic actions within the mouse PAG. This differs to the rat PAG where only μ-opioid receptor actions have been observed