Bias-voltage dependence of the magneto-resistance in ballistic vacuum tunneling: Theory and application to planar Co(0001) junctions

Motivated by first-principles results for jellium and by surface-barrier shapes that are typically used in electron spectroscopies, the bias voltage in ballistic vacuum tunneling is treated in a heuristic manner. The presented approach leads in particular to a parameterization of the tunnel-barrier shape, while retaining a first-principles description of the electrodes. The proposed tunnel barriers are applied to Co(0001) planar tunnel junctions. Besides discussing main aspects of the present scheme, we focus in particular on the absence of the zero-bias anomaly in vacuum tunneling.Comment: 19 pages with 8 figure

Determinants of Functional Coupling between Astrocytes and Respiratory Neurons in the Pre-Bötzinger Complex

Respiratory neuronal network activity is thought to require efficient functioning of astrocytes. Here, we analyzed neuron-astrocyte communication in the pre-Bötzinger Complex (preBötC) of rhythmic slice preparations from neonatal mice. In astrocytes that exhibited rhythmic potassium fluxes and glutamate transporter currents, we did not find a translation of respiratory neuronal activity into phase-locked astroglial calcium signals. In up to 20% of astrocytes, 2-photon calcium imaging revealed spontaneous calcium fluctuations, although with no correlation to neuronal activity. Calcium signals could be elicited in preBötC astrocytes by metabotropic glutamate receptor activation or after inhibition of glial glutamate uptake. In the latter case, astrocyte calcium elevation preceded a surge of respiratory neuron discharge activity followed by network failure. We conclude that astrocytes do not exhibit respiratory-rhythmic calcium fluctuations when they are able to prevent synaptic glutamate accumulation. Calcium signaling is, however, observed when glutamate transport processes in astrocytes are suppressed or neuronal discharge activity is excessive

TRAF6 prevents fatal inflammation by homeostatic suppression of MALT1 protease.

[Figure: see text]