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Biomedical subjects

R Moessner

Publications and source records attributed to R Moessner.

11 recordsLinked to original sources
PubMed2002

Order by distortion and string modes in pyrochlore antiferromagnets.

We study the effects of magnetoelastic couplings on pyrochlore antiferromagnets. We employ Landau theory, extending an investigation begun by Yamashita and Ueda for the case of S = 1, and classical analyses to argue that such couplings generate bond order via a spin-Peierls transition. This is followed by, or concurrent with, a transition into one of several possible low-temperature Néel phases, with most simply collinear, but also coplanar or mixed spin patterns. In a collinear Néel phase, a dispersionless stringlike magnon mode dominates the resulting excitation spectrum, providing a distinctive signature of the parent geometrically frustrated state. We comment on the experimental situation.

Journal Article↗
PubMed2002

Lack of 5-HT(1B) receptor and of serotonin transporter have different effects on the segregation of retinal axons in the lateral geniculate nucleus compared to the superior colliculus.

We have shown previously that raised levels of serotonin (5-hydroxytryptamine or 5-HT) during development prevent retinal ganglion cell axons from segregating into eye-specific regions in their principal targets: the superior colliculus and the dorsal lateral geniculate nucleus. Possible mediators of 5-HT in this system include its plasma membrane transporter, which is transiently expressed by a sub-population of retinal ganglion cells, and the presynaptic 5-HT(1B) receptor carried on retinal ganglion cell axons. We analysed the retinal projections of 5-HT(1B) knockout (n=15), serotonin transporter knockout (n=14), serotonin transporter/5-HT(1B) double knockout (n=4) and monoamine oxidase A/5-HT(1B) double knockout (n=3) mice. In all four different knockout mice, the ipsilateral retinal projection to the superior colliculus was more diffuse and lost its characteristic patchy distribution. The alterations were most severe in the serotonin transporter knockout mice, where the ipsilateral retinal fibres covered the entire rostrocaudal and mediolateral extent of the superior colliculus, whereas in the 5-HT(1B) and double knockout mice, fibres retracted from the caudal and lateral superior colliculus. Abnormalities in the 5-HT(1B) knockout mice appeared only after postnatal day (P) 4. Treatment with parachlorophenylalanine (at P1-P12) to decrease serotonin levels caused an exuberance of the ipsilateral retinal fibres throughout the superior colliculus (n=9). In the dorsal lateral geniculate nucleus in contrast, the distribution and size of the ipsilateral retinal projection was normal in all four knockout mice. In the serotonin transporter knockout mice however, the contralateral retinal fibres failed to retract from the mediodorsal dorsal lateral geniculate nucleus, an abnormality that was reversed by early treatment with parachlorophenylalanine and in the serotonin transporter/5-HT(1B) double knockout. OUR OBSERVATIONS INDICATE: (1) that the lack of 5-HT transporter and the associated changes in 5-HT levels impair the segregation of retinal axons in both the superior colliculus and the dorsal lateral geniculate nucleus; (2) that 5-HT and 5-HT(1B) receptors are necessary for the normal refinement of the ipsilateral retinal fibres in the superior colliculus, but are not essential for the establishment of eye-specific segregation in the thalamus. Thus, both an excess and a lack of 5-HT affect the refinement of the superior colliculus retinal projection, while the establishment of eye-specific patterns in the dorsal lateral geniculate nucleus appears not to be sensitive to the lack of 5-HT or 5-HT(1B) receptors.

Animals↗
PubMed2001

Barrel pattern formation requires serotonin uptake by thalamocortical afferents, and not vesicular monoamine release.

Thalamocortical neurons innervating the barrel cortex in neonatal rodents transiently store serotonin (5-HT) in synaptic vesicles by expressing the plasma membrane serotonin transporter (5-HTT) and the vesicular monoamine transporter (VMAT2). 5-HTT knock-out (ko) mice reveal a nearly complete absence of 5-HT in the cerebral cortex by immunohistochemistry, and of barrels, both at P7 and adulthood. Quantitative electron microscopy reveals that 5-HTT ko affects neither the density of synapses nor the length of synaptic contacts in layer IV. VMAT2 ko mice, completely lacking activity-dependent vesicular release of monoamines including 5-HT, also show a complete lack of 5-HT in the cortex but display largely normal barrel fields, despite sometimes markedly reduced postnatal growth. Transient 5-HTT expression is thus required for barrel pattern formation, whereas activity-dependent vesicular 5-HT release is not.

Aging↗
PubMed2001

Resonating valence bond phase in the triangular lattice quantum dimer model.

We study the quantum dimer model on the triangular lattice, which is expected to describe the singlet dynamics of frustrated Heisenberg models in phases where valence bond configurations dominate their physics. We find, in contrast to the square lattice, that there is a truly short ranged resonating valence bond phase with no gapless excitations and with deconfined, gapped, spinons for a finite range of parameters. We also establish the presence of crystalline dimer phases.

Journal Article↗
PubMed2001

Abnormal trafficking and subcellular localization of an N-terminally truncated serotonin transporter protein.

We report here that a truncated 5-HTT protein is produced in the neurons of the raphe, in serotonin transporter (5-HTT) knockout (KO) mice. The 5-HTT gene has exon 2 deleted and we found that one main transcript, shortened by 450 bp, is produced in these KO mice. The mutated 5-HTT protein is only recognized by antibodies against the C-terminal portion of 5-HTT. This protein is not functional as there is no high-affinity serotonin uptake in 5-HTT KO mice, in adults or during development. Conversely, low-affinity serotonin uptake was detected in vitro, and in dopaminergic neurons of the substantia nigra in vivo. The truncated 5-HTT, recognized by antibodies to the C-terminus, is present exclusively in the somatodendritic compartment of the raphe neurons instead of being exported to axons. As shown with confocal and electron microscopy, the truncated 5-HTT does not reach the plasma membrane and is essentially retained in the endoplasmic reticulum. However, this does not seem to trigger refolding or degradation responses, as no upregulation of the chaperone BiP or of the degradation signal ubiquitin was detected. Last, as observed in heterozygous mice, the presence of the truncated 5-HTT protein, although produced in large quantities, does not disturb the normal trafficking of the wild-type protein. This study therefore validates the 5-HTT KO model despite the occurrence of an incomplete translation, and brings novel information on the in vivo 5-HT uptake and cellular processing of an abnormal 5-HTT protein.

Animals↗
PubMed2000

Two-dimensional periodic frustrated ising models in a transverse field

We investigate the interplay of classical degeneracy and quantum dynamics in a range of periodic frustrated transverse field Ising systems at zero temperature. We find that such dynamics can lead to unusual ordered phases and phase transitions or to a quantum spin liquid (cooperative paramagnetic) phase as in the triangular and kagome lattice antiferromagnets, respectively. For the latter, we further predict passage to a bond-ordered phase followed by a critical phase as the field is tilted. These systems also provide exact realizations of quantum dimer models introduced in studies of high temperature superconductivity.

Journal Article↗
PubMed1999

Adaptive changes of serotonin 5-HT2A receptors in mice lacking the serotonin transporter.

The serotonin transporter (5-HTT) plays a key-role in the control of serotoninergic neurotransmission and is the target of some antidepressants. Possible adaptive changes in brain 5-HT2A receptors were investigated in knock-out mice that do not express the 5-HTT. Autoradiographic labeling of these receptors by the selective antagonist [3H]MDL 100,907 and saturation experiments with cortical membranes revealed: (1) a new localization of these receptors in the external field of striatum (possibly in striosomes); (2) regional variations in adaptive changes in the density of 5-HT2A receptors in 5-HT(-/-) mutants (-30-40% in the claustrum, cerebral cortex and lateral striatum; no significant change in the striatum core) as compared to wild-type mice.

Adaptation, Physiological↗
PubMed1999

Mechanisms of deficient interferon-gamma production in atopic diseases.

BACKGROUND: The mechanisms responsible for an imbalanced cytokine response in atopic diseases are still not understood. While impaired interferon-gamma (IFN-gamma) production may be the result of a pathological T-cell/antigen-presenting cell (APC) interaction, evidence was provided that the T cell itself may have an intrinsic defect to produce IFN-gamma. OBJECTIVE: To clarify whether impaired IFN-gamma production by T cells from patients with atopic dermatitis (AD) represents an intrinsic defect in producing IFN-gamma. METHODS: Effector T cells were generated from CD4+ CD45RA+-naive precursors from patients with AD and healthy control individuals by activation with anti-CD3+ anti-CD28 MoAbs. Following restimulation, IFN-gamma production was measured by ELISA and flow cytometry. RESULTS: IFN-gamma production by atopic T cells was decreased compared with healthy T cells. IL-12 present at priming or high doses of IL-2 during the culture period, even in the absence of IL-12, completely restored IFN-gamma production. Conversion of naive CD45RA+ to CD45R0+ effector cells did not differ between atopic and healthy donors' T cells. CONCLUSION: Impaired IFN-gamma production by T cells from atopic individuals is not the result of an intrinsic, genetically fixed, defect to produce sufficient amounts of IFN-gamma. The data provides evidence that correction of an impaired TH1 response in AD may be successful at the precursor T cell level.

Adolescent↗
PubMed1988

The MRC OX-45 antigen of rat leukocytes and endothelium is in a subset of the immunoglobulin superfamily with CD2, LFA-3 and carcinoembryonic antigens.

The MRC OX-45 cell surface antigen is a glycoprotein of 45,000 apparent mol. wt of rat leukocytes and endothelium. Antibodies against the antigen inhibit T lymphocyte responses by stimulation of suppression by accessory cells. We now report the immunochemical characterization of this antigen and its cDNA sequence. The predicted protein sequence contains 240 amino acids including a leader sequence of 22 residues and a carboxy-terminal sequence of 23 residues that is replaced in the processed molecule by a glycosyl-phosphatidylinositol anchor attached at serine 195. Two Ig-related domains are predicted to account for all of the processed sequence and the circular dichroism spectrum shows pure beta-structure. The amino-terminal domain is V-like, but without a disulphide bond, while the second domain is C-like (C2-SET) with two disulphide bonds. The sequence matches particularly well with the extracellular parts of LFA-3 and CD2 antigens and the first two domains of carcinoembryonic antigen and non-specific, cross-reacting antigen.

Animals↗