Scattering amplitudes of massive Nambu-Goldstone bosons

Massive Nambu-Goldstone (mNG) bosons are quasiparticles the gap of which is determined exactly by symmetry. They appear whenever a symmetry is broken spontaneously in the ground state of a quantum many-body system and at the same time explicitly by the system’s chemical potential. In this paper, we revisit mNG bosons and show that apart from their gap symmetry also protects their scattering amplitudes. Just like for ordinary gapless Nambu-Goldstone (NG) bosons, the scattering amplitudes of mNG bosons vanish in the long-wavelength limit. Unlike for gapless NG bosons, this statement holds for any scattering process involving one or more external mNG states; there are no kinematic singularities associated with the radiation of a soft mNG boson from an on-shell initial or final state.publishedVersio

Scattering theory of transport through disordered magnets

We present a scattering theory of transport through noncollinear disordered magnetic insulators. For concreteness, we study and compare the random field model (RFM) and the random anisotropy model (RAM). The RFM and RAM are used to model random spin disorder systems and amorphous materials, respectively. We utilize the Landauer-Buttiker formalism to compute the transmission probability and spin conductance of one-dimensional disordered spin chains. The RFM and the RAM both exhibit Anderson localization, which means that the transmission probability and spin conductance decay exponentially with the system length. We define two localization lengths based on the transmission probability and the spin conductance, respectively. Next, we numerically determine the relationship between the localization lengths and the strength of the disorder. In the limit of weak disorder, we find that the localization lengths obey power laws and determine the critical exponents. Our results are expressed via the universal exchange length and are therefore expected to be general

Effects of 4-methylimidazole on cerebral glutamate decarboxylase activity and specific GABA receptor binding in mice

4-Methylimidazole (4MeI) is a tremorogenic and convulsive agent of concern both in human and veterinary toxicology. The in vitro effects of 4MeI (5 μM–20 mM) on cerebral glutamate decarboxylase (GAD) activity and (in concentrations up to 50 mM) on binding of [3H]GABA to cerebral GABA receptors were tested in brain tissue from B6D2 mice. The effects of 1-methylimidazole (1MeI), 2-methylimidazole (2MeI), 4-methylhydroxy-imidazole (4MeOHI), imidazole-4-aceticacid (4AcI) (all in concentrations of 5–20 mM) and imidazole (20 mM) on GAD activity were also tested. In addition, the effect of a lethal dose of 4MeI (250 mg/kg ip) to B6D2 mice in vivo on the postmortem concentrations of γ-aminobutyric acid (GABA) and glutamate in their brains were measured. In all experiments, student's t-test was used for statistical comparison. 4MeI in concentrations of 2 mM and above did inhibit GAD activity significantly in vitro, but glutamate and GABA concentrations in mouse brains after lethal 4MeI poisoning were not significantly different from control values. The effect of 2MeI on GAD activity was stronger than the effect of 4MeI. Binding of [3H]GABA to cerebral GABA receptors in vitro was significantly inhibited only at 4MeI concentrations of 5 mM and above. The results indicate that neither inhibition of GABA synthesis nor competitive inhibition of the binding of GABA to its receptors are likely mechanisms for the excitation and convulsions seen in 4MeI poisoning in animals

250-MHz synchronously pumped optical parametric oscillator at 2.25-2.6 {\mu}m and 4.1-4.9 {\mu}m

A compact and versatile femtosecond mid-IR source is presented, based on an optical parametric oscillator (OPO) synchronously pumped by a commercial 250-MHz Er:fiber laser. The mid-IR spectrum can be tuned in the range 2.25-2.6 \mu m (signal) and 4.1-4.9 \mu m (idler), with average power from 20 to 60 mW. At 2.5 \mu m a minimum pulse duration of 110 fs and a power of 40 mW have been obtained. Active stabilization of the OPO cavity length has been achieved in the whole tuning range

Effects of hippocampal damage on reward threshold and response rate during self-stimulation of the ventral tegmental area in the rat

The main purpose of this study was to explore the role of the hippocampus in motivated behavior. Rats with bilateral excitotoxic lesions of the hippocampus and controls were trained to lever press for electrical stimulation of the ventral tegmental area. Rate intensity functions were generated from an ascending and descending series of current intensities. Lesion-induced changes in sensitivity to reward were distinguished from enhancements in motor output by calculating reward thresholds and maximal response rates from the rate-intensity functions. Rats with hippocampal damage showed lower reward thresholds and higher maximal response rates than controls. These results provide further evidence of hippocampal modulation of the nucleus accumbens, suggesting that lesions of this structure enhance sensitivity to reward and increase motor output

Excitotoxic Brain Injury Suppresses Striatal High-Affinity Glutamate Uptake in Perinatal Rats

In immature rodent brain, the glutamate receptor agonist N -methyl-D-aspartate (NMDA) is a potent neurotoxin. In postnatal day (PND)-7 rats, intrastriatal injection of 25 nmol of NMDA results in extensive ipsilateral forebrain injury. In this study, we examined alterations in high-affinity [ 3 H]glutamate uptake (HAGU) in NMDA-lesioned striatum. HAGU was assayed in synaptosomes, prepared from lesioned striatum, the corresponding contralateral striatum, or unlesioned controls. Twenty-four hours after NMDA injection (25 nmol), HAGU declined 44 ± 8% in lesioned tissue, compared with the contralateral striatum (mean ± SEM, n = 6 assays, p < 0.006, paired t test). Doses of 5–25 nmol of NMDA resulted in increasing suppression of HAGU (5 nmol, n = 3; 12.5 nmol, n = 3; and 25 nmol, n = 5 assays; p < 0.01, regression analysis). The temporal evolution of HAGU suppression was biphasic. There was an early transient suppression of HAGU (−28 ± 4% at 1 h; p < 0.03, analysis of variance, comparing changes at 0.5, 1, 2, and 3 h after lesioning); 1 or 5 days postinjury there was sustained loss of HAGU (at 5 days, −56 ± 11%, n = 3, p < 0.03, paired t test, lesioned versus contralateral striata). Treatment with the noncompetitive NMDA antagonist MK-801 (1 mg/kg i.p.) attenuated both the early and subsequent irreversible suppression of HAGU (1 h postlesion −28 ± 4%, n = 6 assays versus −12.6 ± 5% with MK-801, n = 4, p = 0.005; 24 h postlesion, −44 ± 8%, n = 5, versus +2.4 ± 6%, n = 3 with MK-801, p = 0.01, Wilcoxon ranked sum tests). In immature brain excitotoxic lesions produce an acute reversible suppression of HAGU, and a delayed long-lasting reduction in HAGU secondary to brain injury. These data suggest that accumulation of endogenous glutamate, as a consequence of the acute disruption of HAGU, could contribute to the pathogenesis of excitotoxic neuronal injury.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65556/1/j.1471-4159.1991.tb02011.x.pd

Behavioural and biochemical effects of an ICV injection of streptozotocin in old Lewis rats

Intacerebroventricularly (ICV) injected streptozotocin (STREP) decreases central glucose metabolism and energy metabolism, which has also been observed in patients with dementia. In the present study we examined the behavioral (open-field behavior and two-way active avoidance learning) and biochemical (hippocampal ChAT activity) effects of STREP treatment in old Lewis rats. The results suggest that hippocampal function was affected by STREP. STREP-treated rats acquired the two-way active avoidance task faster than the control rats, which indicates that STREP treatment does not lead to a general learning deficit. Hippocampal ChAT activity was decreased in STREP-treated rats. The present results suggests also that susceptibility to STREP amy not be related to age in Lewis rats

Perinatal Hypoxia-Ischemia Disrupts Striatal High-Affinity [ 3 H]Glutamate Uptake into Synaptosomes

: We examined the impact of hypoxia-ischemia on high-affinity [ 3 H]glutamate uptake into a synaptosomal fraction prepared from immature rat corpus striatum. In 7-day-old pups the right carotid artery was ligated, and pups were exposed to 8% oxygen for 0, 0.5, 1, or 2.5 h, and allowed to recover for up to 24 h before they were killed. High-affinity glutamate uptakes in striatal synaptosomes derived from tissue ipsilateral and contralateral to ligation were compared. After 1 h of hypoxia plus ischemia, high-affinity glutamate uptake in the striatum was reduced by 54 ± 13% compared with values from the opposite (nonischemic) side of the brain (p < 0.01, t test versus ligates not exposed to hypoxia). There were similar declines after 2.5 h of hypoxiaischemia. Activity remained low after a 1 h recovery period in room air, but after 24 h of recovery, high-affinity glutamate uptake was equal bilaterally. Kinetic analysis revealed that loss of activity could be attributed primarily to a 40% reduction in the number of uptake sites. Hypoxia alone had no effect on high-affinity glutamate uptake although it reduced synaptosomal uptake of [ 3 H]3,4-dihydroxyphenyl-ethylamine. Addition of 1 mg/ml of bovine serum albumin to the incubation medium preferentia'ly stimulated high-affinity glutamate uptake in hypoxic-ischemic brain compared with its effects in normal tissue. These studies demonstrate that hypoxia-ischemia reversibly inhibits high-affinity glutamate uptake and this occurs earlier than the time required to produce neuronal damage in the model.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66361/1/j.1471-4159.1986.tb00803.x.pd

Flow-orthogonal bead oscillation in a microfluidic chip with a magnetic anisotropic flux-guide array

A new concept for the manipulation of superparamagnetic beads inside a microfluidic chip is presented in this paper. The concept allows for bead actuation orthogonal to the flow direction inside a microchannel. Basic manipulation functionalities were studied by means of finite element simulations and results were oval-shaped steady state oscillations with bead velocities up to 500 μm/s. The width of the trajectory could be controlled by prescribing external field rotation. Successful verification experiments were performed on a prototype chip fabricated with excimer laser ablation in polycarbonate and electroforming of nickel flux-guides. Bead velocities up to 450 μm/s were measured in a 75 μm wide channel. By prescribing the currents in the external quadrupole magnet, the shape of the bead trajectory could be controlled

Inhibition of vesicular glutamate storage and exocytotic release by Rose Bengal

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65725/1/j.1471-4159.2001.00200.x.pd