Glucose availability and sensitivity to anoxia of isolated rat peripheral nerve

The contrast between resistance to ischemia and ischemic lesions in peripheral nerves of diabetic patients was explored by in vitro experiments. Isolated and desheathed rat peroneal nerves were incubated in the following solutions with different glucose availability: 1) 25 mM glucose, 2) 2.5 mM glucose, and 3) 2.5 mM glucose plus 10 mM 2-deoxy-D-glucose. Additionally, the buffering power of all of these solutions was modified. Compound nerve action potential (CNAP), extracellular pH, and extracellular potassium activity (aKe) were measured simultaneously before, during, and after a period of 30 min of anoxia. An increase in glucose availability led to a slower decline in CNAP and to a smaller rise in aKe during anoxia. This resistance to anoxia was accompanied by an enhanced extracellular acidosis. Postanoxic recovery of CNAP was always complete in 25 mM HCO3(-)-buffered solutions. In 5 mM HCO3- and in HCO3(-)-free solutions, however, nerves incubated in 25 mM glucose did not recover functionally after anoxia, whereas nerves bathed in solutions 2 or 3 showed a complete restitution of CNAP. We conclude that high glucose availability and low PO2 in the combination with decreased buffering power and/or inhibition of HCO3(-)-dependent pH regulation mechanisms may damage peripheral mammalian nerves due to a pronounced intracellular acidosis

Changes in extracellular pH during electrical stimulation of isolated rat vagus nerve

Double-barrelled pH-sensitive micro-electrodes were used to record changes of extracellular pH during repetitive stimulation of isolated rat vagus nerves. It was found that a small initial alkaline shift was followed by a prolonged acidification. The acidification was correlated in time with the poststimulus undershoot of the extracellular K+ activity and with the recovery phase of the nerve conduction velocity. In the presence of ouabain, the acid component of the pH change was completely abolished (indicating a metabolic origin), whereas the alkaline component remained unaltered. These pH changes were too small to make a significant contribution to the activity-related changes in conduction velocity of the vagal C-fibres

A test to determine the site of abnormal neuromuscular refractoriness

Objective: The relative refractory period (RRP) of motor axons is an important parameter in nerve excitability tests of the recovery cycle (RC). Abnormalities may have a site in the axonal membrane, the neuromuscular junction, or in a dysfunction of the muscle. We aimed in this study to determine the site of abnormality, using a modified protocol of the conventional RC test, whereby an additional supramaximal stimulus is added at the same interstimulus interval as in RC recordings (RCSM). Methods: Twenty-four healthy subjects aged 37.8 ± 2.4 years (mean ± SE) were examined with median nerve excitability testing using RC and RCSM protocols at normal temperature (34.1 ± 0.2 °C). The recordings were repeated in 12 subjects after selective cooling of the thenar muscle (25.2 ± 0.7 °C) and in 12 subjects after cooling the nerve trunk at the wrist (24.9 ± 0.3 °C). Results: After cooling the nerve, RRP measured with RC and RCSM were prolonged similarly (medians by 1.8 ms, and 2.1 ms respectively). In contrast, cooling the muscle prolonged RRP measured with RC (by 1.3 ms), but did not significantly prolong RRP measured with RCSM. RRPs measured by RC and RCSM were significantly different when cooling was at the muscle (P = 5.10-4), but not when cooling was at the nerve (P = 0.57). Conclusions: A difference between RC and RCSM indicates abnormal excitability distal to the axonal membrane under the stimulating electrode. Significance: Combining RCSM with the conventional RC protocol should help to localize the site of abnormal neuromuscular refractoriness

Adenosine, ‘pertussis-sensitive’ G-proteins, and K+ conductance in central mammalian neurones under energy deprivation

There is a striking similarity between the effects of adenosine and of hypoxia or glucose depletion on membrane potential and conductance of hippocampal neurones in tissue slices of rat brain. Both induce a membrane hyperpolarization by an increase in potassium conductance. It seemed likely, therefore, that a rise in extracellular adenosine concentration during energy deprivation may link neuronal metabolism with membrane K+ conductance. To test this hypothesis, we have now investigated the effects of hypoxia/glucose deprivation on hippocampal neurones from pertussis toxin-treated rats. In such slices adenosine had no effect on postsynaptic membrane potential and input resistance. Nevertheless, hypoxia or glucose depletion were as effective as in controls. These data provide evidence against adenosine as the main mediator between cell metabolism and potassium conductance

AC susceptibility investigation of vortex dynamics in nearly-optimally doped REFeAsO1−x_{1-x}Fx_{x} superconductors (RE = La, Ce, Sm)

Ac susceptibility and static magnetization measurements were performed in the nearly-optimally doped LaFeAsO$_{0.9}$F$_{0.1}$ and CeFeAsO$_{0.92}$F$_{0.08}$ superconductors, complementing earlier results on SmFeAsO$_{0.8}$F$_{0.2}$ [Phys. Rev. {\bf B 83}, 174514 (2011)]. The magnetic field -- temperature phase diagram of the mixed superconducting state is drawn for the three materials, displaying a sizeable reduction of the liquid phase upon increasing $T_{c}$ in the range of applied fields ($H \leq 5$ T). This result indicates that SmFeAsO$_{0.8}$F$_{0.2}$ is the most interesting compound among the investigated ones in view of possible applications. The field-dependence of the intra-grain depinning energy $U_{0}$ exhibits a common trend for all the samples with a typical crossover field value (2500 Oe $\lesssim H_{cr} \lesssim 5000$ Oe) separating regions where single and collective depinning processes are at work. Analysis of the data in terms of a simple two-fluid picture for slightly anisotropic materials allows to estimate the zero-temperature penetration depth $\lambda_{ab}(0)$ and the anisotropy parameter $\gamma$ for the three materials. Finally, a sizeable suppression of the superfluid density is deduced in a $s^{\pm}$ two-gap scenario

A chloride channel in rat and human axons

Current recordings from single chloride channels were obtained from excised and cell-attached patches of rat and human axons. In rat axons the channels showed an outwardly rectifying current-voltage relationship with a slope conductance of 33 pS at negative membrane potentials and 65 pS at positive potentials (symmetrical 150 mM CsCl). They were measurably for cations (PNa/PCs/PCl=0.1/0.2/1). Channel currents were independent of cytoplasmatic calcium concentration. Inactivation was not observed and gating was weakly voltage dependent. Cl− channels in human axons showed similar gating behavior but had a lower conductance

Disorder-induced Spin Gap in the Zigzag Spin-1/2 Chain Cuprate Sr_{0.9}Ca_{0.1}CuO_2

We report a comparative study of 63Cu Nuclear Magnetic Resonance spin lattice relaxation rates, T_1^{-1}, on undoped SrCuO_2 and Ca doped Sr_{0.9}Ca_{0.1}CuO_2 spin chain compounds. A temperature independent T_1^{-1} is observed for SrCuO_2 as expected for an S=1/2 Heisenberg chain. Surprisingly, we observe an exponential decrease of T_1^{-1} for T < 90,K in the Ca-doped sample evidencing the opening of a spin gap. The data analysis within the J_1-J_2 Heisenberg model employing density-matrix renormalization group calculations suggests an impurity driven small alternation of the J_2-exchange coupling as a possible cause of the spin gap.Comment: 4 pages, 4 figure

Muscle action potential scans and ultrasound imaging in neurofibromatosis type 2

INTRODUCTION: The neuropathy in patients with neurofibromatosis type 2 (NF2) is difficult to quantify and follow up. In this study we compared 3 methods that may help assess motor axon pathology in NF2 patients. METHODS: Nerve conduction studies in median nerves were supplemented by deriving motor unit number estimates (MUNEs) from compound muscle action potential (CMAP) scans and by high-resolution ultrasound (US) peripheral nerve imaging. RESULTS: CMAP amplitudes and nerve conduction velocity were normal in the vast majority of affected individuals, but CMAP scan MUNE revealed denervation and reinnervation in many peripheral nerves. In addition, nerve US imaging enabled monitoring of the size and number of schwannoma-like fascicular enlargements in median nerve trunks. CONCLUSION: In contrast to conventional nerve conduction studies, CMAP scan MUNE in combination with US nerve imaging can quantify the NF2-associated neuropathy and may help to monitor disease progression and drug treatments