ABSTRACT
High-resolution neutron and THz spectroscopies are used to study the magnetic excitation spectrum of Cs_{2}CoBr_{4}, a distorted-triangular-lattice antiferromagnet with nearly XY-type anisotropy. What was previously thought of as a broad excitation continuum [L. Facheris et al., Phys. Rev. Lett. 129, 087201 (2022)PRLTAO0031-900710.1103/PhysRevLett.129.087201] is shown to be a series of dispersive bound states reminiscent of "Zeeman ladders" in quasi-one-dimensional Ising systems. At wave vectors where interchain interactions cancel at the mean field level, they can indeed be interpreted as bound finite-width kinks in individual chains. Elsewhere in the Brillouin zone their true two-dimensional structure and propagation are revealed.
Subject(s)
Memory , Neutrons , Anisotropy , ReproductionABSTRACT
We report an excellent realization of the highly nonclassical incommensurate spin-density wave (SDW) state in the quantum frustrated antiferromagnetic insulator Cs_{2}CoBr_{4}. In contrast to the well-known Ising spin chain case, here the SDW is stabilized by virtue of competing planar in-chain anisotropies and frustrated interchain exchange. Adjacent to the SDW phase is a broad m=1/3 magnetization plateau that can be seen as a commensurate locking of the SDW state into the up-up-down (UUD) spin structure. This represents the first example of the long-sought SDW-UUD transition in triangular-type quantum magnets.
ABSTRACT
By testing the effect of spermine on N-methyl-D-aspartate (NMDA)-evoked [3H]noradrenaline release in rat hippocampal slices, we revealed a presynaptic spermine-sensitive NMDA receptor most probably localized on noradrenergic terminals. Spermine (1 mM), per se totally inactive, was able to reverse the tetrodotoxin-induced blockade of the NMDA effect, restoring tritium efflux to approximately 50% of the NMDA-evoked release measured in the absence of tetrodotoxin. This effect was partially antagonized by D(-)-2-amino-7-phosphonoheptanoic acid. Our results may help to elucidate the role that spermine exerts on excitatory amino acids receptors.
Subject(s)
Receptors, N-Methyl-D-Aspartate/drug effects , Spermine/pharmacology , Tetrodotoxin/pharmacology , Animals , Hippocampus/drug effects , Hippocampus/metabolism , In Vitro Techniques , Male , Norepinephrine/metabolism , Rats , Rats, Inbred StrainsABSTRACT
By monitoring dopamine metabolism in rat pheochromocytoma derived PC12 cell cultures during extended treatment with manganese chloride, we assessed the functional changes occurring in a dopaminergic system during the development of manganese-induced damage. Besides eliciting a specific toxic effect on PC12 cells, manganese induced the complete disappearance of extracellular (free) but not intracellular (vesicle stored) dopamine and its metabolite 3,4-dihydroxyphenylacetic acid. This effect was observed also using low manganese concentrations (1 microM) and mainly occurred by non-enzymatic catechol oxidation since it was still evident in a cell free medium and it was fully prevented by ascorbic acid but not by reduced glutathione. The possibility of a mere "non-biological" action was ruled out by the observation of an irreversible effect of manganese as manifested by the cells' apparent inability to release dopamine or 3,4-dihydroxyphenylacetic acid into the culture medium even after complete manganese removal (post-manganese incubation). That a free radical mechanism was not involved in the genesis of this irreversible effect was shown by the fact that neither ascorbic acid, catalase, superoxide dismutase nor glutathione-peroxidase were able to prevent the decrease in catecholamine levels in the "post-manganese" incubation medium when added at the same time as the manganese. The results establish this PC12 cell system as an in vitro model for studying interactions between manganese and catechols and provide a detailed description of the nature of the neurochemical alterations that this heavy metal can induce in a dopaminergic system.