Josephson Coupling and Fiske Dynamics in Ferromagnetic Tunnel Junctions

We report on the fabrication of Nb/AlO_x/Pd_{0.82}Ni_{0.18}/Nb superconductor/insulator/ferromagnetic metal/superconductor (SIFS) Josephson junctions with high critical current densities, large normal resistance times area products, high quality factors, and very good spatial uniformity. For these junctions a transition from 0- to \pi-coupling is observed for a thickness d_F ~ 6 nm of the ferromagnetic Pd_{0.82}Ni_{0.18} interlayer. The magnetic field dependence of the \pi-coupled junctions demonstrates good spatial homogeneity of the tunneling barrier and ferromagnetic interlayer. Magnetic characterization shows that the Pd_{0.82}Ni_{0.18} has an out-of-plane anisotropy and large saturation magnetization, indicating negligible dead layers at the interfaces. A careful analysis of Fiske modes provides information on the junction quality factor and the relevant damping mechanisms up to about 400 GHz. Whereas losses due to quasiparticle tunneling dominate at low frequencies, the damping is dominated by the finite surface resistance of the junction electrodes at high frequencies. High quality factors of up to 30 around 200 GHz have been achieved. Our analysis shows that the fabricated junctions are promising for applications in superconducting quantum circuits or quantum tunneling experiments.Comment: 15 pages, 9 figure

Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury.

We show that transsynaptic apoptosis is induced in the superficial dorsal horn (laminas I-III) of the spinal cord by three distinct partial peripheral nerve lesions: spared nerve injury, chronic constriction, and spinal nerve ligation. Ongoing activity in primary afferents of the injured nerve and glutamatergic transmission cause a caspase-dependent degeneration of dorsal horn neurons that is slow in onset and persists for several weeks. Four weeks after spared nerve injury, the cumulative loss of dorsal horn neurons, determined by stereological analysis, is >20%. GABAergic inhibitory interneurons are among the neurons lost, and a marked decrease in inhibitory postsynaptic currents of lamina II neurons coincides with the induction of apoptosis. Blocking apoptosis with the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) prevents the loss of GABAergic interneurons and the reduction of inhibitory currents. Partial peripheral nerve injury results in pain-like behavioral changes characterized by hypersensitivity to tactile or cold stimuli. Treatment with zVAD, which has no intrinsic analgesic properties, attenuates this neuropathic pain-like syndrome. Preventing nerve injury-induced apoptosis of dorsal horn neurons by blocking caspase activity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity