Realization of Translational Symmetry in Trapped Cold Ion Rings.

We crystallize up to 15 ^{40}Ca^{+} ions in a ring with a microfabricated silicon surface Paul trap. Delocalization of the Doppler laser-cooled ions shows that the translational symmetry of the ion ring is preserved at millikelvin temperatures. By characterizing the collective motion of the ion crystals, we identify homogeneous electric fields as the dominant symmetry-breaking mechanism at this energy scale.

RGS proteins maintain robustness of GPCR-GIRK coupling by selective stimulation of the G protein subunit Gαo.

Termination of heterotrimeric guanine nucleotide-binding protein (G protein) signaling downstream of activated G protein-coupled receptors (GPCRs) is accelerated by regulator of G protein signaling (RGS) proteins, which act as guanosine triphosphatase (GTPase)-activating proteins (GAPs). Using a Xenopus oocyte expression system, we found that although RGS proteins had a negative effect of accelerating the kinetics of GPCR-coupled potassium ion (K+) channel (GIRK) deactivation, they also had positive effects of increasing the amplitudes and activation kinetics of neurotransmitter-evoked GIRK currents. The RGS box domain alone was sufficient to stimulate neurotransmitter-dependent activation of GIRK currents.

Induction of TRPV1 desensitization by a biased receptor agonist.

Selective suppression of hyperactive sensory neurons is an attractive strategy for managing pathological pain. Blocking Na(+) channels to eliminate action potentials and desensitizing transduction channels can both reduce sensory neuron excitability. The novel synthetic vanilloid ligand cap-ET preserves agonist activation of intracellular Ca(2+) signals and large organic cation transport but loses effective electric current induction.

Activity-dependent targeting of TRPV1 with a pore-permeating capsaicin analog.

The capsaicin receptor TRPV1 is the principal transduction channel for nociception. Excessive TRPV1 activation causes pathological pain. Ideal pain mangement requires selective inhibition of hyperactive pain-sensing neurons, but sparing normal nociception.