No abstract

Nonlinear two-photon photoemission electron microscopy is used to image surface plasmon polariton (SPP) wave packets excited by an obliquely incident laser pulse (~10 fs) at a single slit fabricated in a thin silver film. We image the forward propagating polarization grating formed by the coherent superposition of the external excitation pulse and the SPP wave packet fields. By systematically varying the coupling slit width from sub-to multiple-wavelength scale, we observe a modulated increase of the grating intensity, which is phenomenologically accounted for by distinct contributions to the forward coupling efficiency from the incident to the SPP waves. Full-wave, vectorial finite-difference time-domain (FDTD) simulation of the experiments is in good agreement with the experimental observations and explains their origin. In particular, the FDTD simulation illustrates detailed spatial variation of the polarization grating as a function of the geometry of the slit under excitation by ultrafast laser pulses at an oblique incidence.2

Objective The peripheral myelin protein-22 (PMP22) gene is associated with the most common types of inherited neuropathies, including hereditary neuropathy with liability to pressure palsies (HNPP) caused by PMP22 deficiency. However, the function of PMP22 has yet to be defined. Our previous study has shown that PMP22 deficiency causes an impaired propagation of nerve action potentials in the absence of demyelination. In the present study, we tested an alternative mechanism relating to myelin permeability. Methods Utilizing Pmp22+/− mice as a model of HNPP, we evaluated myelin junctions and their permeability using morphological, electrophysiological, and biochemical approaches. Results We show disruption of multiple types of cell junction complexes in peripheral nerve, resulting in increased permeability of myelin and impaired action potential propagation. We further demonstrate that PMP22 interacts with immunoglobulin domain–containing proteins known to regulate tight/adherens junctions and/or transmembrane adhesions, including junctional adhesion molecule-C (JAM-C) and myelin-associated glycoprotein (MAG). Deletion of Jam-c or Mag in mice recapitulates pathology in HNPP. Interpretation Our study reveals a novel mechanism by which PMP22 deficiency affects nerve conduction not through removal of myelin, but through disruption of myelin junctions.