Two-Pion Exchange in Proton-Proton Scattering

The contribution of the box and crossed two-pion-exchange diagrams to proton-proton scattering at 90$^{\circ}_{c.m.}$ is calculated in the laboratory momentum range up to 12 GeV/c. Relativistic form factors related to the nucleon and pion size and representing the pion source distribution based on the quark structure of the hadronic core are included at each vertex of the pion-nucleon interaction. These form factors depend on the four-momenta of the exchanged pions and scattering nucleons. Feynman-diagram amplitudes calculated without form factors are checked against those derived from dispersion relations. In this comparison, one notices that a very short-range part of the crossed diagram, neglected in dispersion-relation calculations of the two-pion-exchange nucleon-nucleon potential, gives a sizable contribution. In the Feynman-diagram calculation with form factors the agreement with measured spin-separated cross sections, as well as amplitudes in the lower part of the energy range considered, is much better for pion-nucleon pseudo-vector vis \`a vis pseudo-scalar coupling. While strengths of the box and crossed diagrams are comparable for laboratory momenta below 2 GeV/c, the crossed diagram dominates for larger momenta, largely due to the kinematics of the crossed diagram allowing a smaller momentum transfer in the nucleon center of mass. An important contribution arises from the principal-value part of the integrals which is non-zero when form factors are included. It seems that the importance of the exchange of color singlets may extend higher in energy than expected

Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS

Hyperexcitability has been suggested to contribute to motoneuron degeneration in amyotrophic lateral sclerosis (ALS). If this is so, and given that the physiological type of a motor unit determines the relative susceptibility of its motoneuron in ALS, then one would expect the most vulnerable motoneurons to display the strongest hyperexcitability prior to their degeneration, whereas the less vulnerable should display a moderate hyperexcitability, if any. We tested this hypothesis in vivo in two unrelated ALS mouse models by correlating the electrical properties of motoneurons with their physiological types, identified based on their motor unit contractile properties. We found that, far from being hyperexcitable, the most vulnerable motoneurons become unable to fire repetitively despite the fact that their neuromuscular junctions were still functional. Disease markers confirm that this loss of function is an early sign of degeneration. Our results indicate that intrinsic hyperexcitability is unlikely to be the cause of motoneuron degeneration

Tractability in Constraint Satisfaction Problems: A Survey

International audienceEven though the Constraint Satisfaction Problem (CSP) is NP-complete, many tractable classes of CSP instances have been identified. After discussing different forms and uses of tractability, we describe some landmark tractable classes and survey recent theoretical results. Although we concentrate on the classical CSP, we also cover its important extensions to infinite domains and optimisation, as well as #CSP and QCSP

Mixed mode oscillations in mouse spinal motoneurons arise from a low excitability state

We explain the mechanism that elicits the mixed mode oscillations (MMOs) and the subprimary firing range that we recently discovered in mouse spinal motoneurons. In this firing regime, high-frequency subthreshold oscillations appear a few millivolts below the spike voltage threshold and precede the firing of a full blown spike. By combining intracellular recordings in vivo (including dynamic clamp experiments) in mouse spinal motoneurons and modeling, we show that the subthreshold oscillations are due to the spike currents and that MMOs appear each time the membrane is in a low excitability state. Slow kinetic processes largely contribute to this low excitability. The clockwise hysteresis in the I–F relationship, frequently observed in mouse motoneurons, is mainly due to a substantial slow inactivation of the sodium current. As a consequence, less sodium current is available for spiking. This explains why a large subprimary range with numerous oscillations is present in motoneurons displaying a clockwise hysteresis. In motoneurons whose I–F curve exhibits a counterclockwise hysteresis, it is likely that the slow inactivation operates on a shorter time scale and is substantially reduced by the de-inactivating effect of the afterhyperpolarization (AHP) current, thus resulting in a more excitable state. This accounts for the short subprimary firing range with only a few MMOs seen in these motoneurons. Our study reveals a new role for the AHP current that sets the membrane excitability level by counteracting the slow inactivation of the sodium current and allows or precludes the appearance of MMOs