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- Kuiper, Pieter, 1960-, et al.
(författare)
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Polarization-dependent nickel 2p x-ray-absorption spectra of La2NiO4+δ
- 1998
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Ingår i: Physical Review B Condensed Matter. - College Park, MD : American Physical Society. - 0163-1829 .- 1095-3795. ; 57:3, s. 1552-1557
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Tidskriftsartikel (refereegranskat)abstract
- We present polarization dependent x-ray-absorption spectra at nickel L edges of well-characterized La2NiO4+δ single crystals. In the stoichiometric compound the splitting between the x2−y2 and the 3z2−r2 orbitals is 0.7 eV, according to a fit of the 2p53d9 multiplet to the spectra. This value is in agreement with an assignment of dd excitations of the optical spectrum. The Ni L edges of the doped compound are consistent with the isotropic prepeak observed at the oxygen 1s edge. Theory does not predict holes on the apex oxygens, but we argue that doping causes a polaronic deformation which reduces the tetragonal distortion of the NiO6 octahedra, and delocalizes the hole over all six ligands.
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| 2. |
- Fundin, Bengt, et al.
(författare)
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Differential dependency of developing mechanoreceptors on neurotrophins, trk receptors, and p75LNGFR
- 1997
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Ingår i: Developmental Biology. - 0012-1606 .- 1095-564X. ; 190:1, s. 94-116
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Tidskriftsartikel (refereegranskat)abstract
- The impact of null mutations of the genes for the NGF family of neurotrophins and their receptors was examined among the wide variety of medium to large caliber myelinated mechanoreceptors which have a highly specific predictable organization in the mystacial pad of mice. Immunofluorescence with anti-protein gene product 9.5, anti-200-kDa neurofilament protein (RT97), and anti-calcitonin gene-related product was used to label innervation in mystacial pads from mice with homozygous null mutations for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), the three tyrosine kinase receptors (trkA, trkB, trkC), and the low-affinity nerve growth factor receptor p75. Specimens were sacrificed at birth and at 1, 2, and 4 weeks for each type of mutation as well as at 11 weeks and 1 year for p75 and trkC mutations, respectively. Our results demonstrate several major concepts about the role of neurotrophins in the development of cutaneous mechanoreceptors that are supplied by medium to large caliber myelinated afferents. First, each of the high-affinity tyrosine kinase receptors, trkA, trkB, and trkC, as well as the low-affinity p75 receptor has an impact on at least one type of mechanoreceptor. Second, consistent with the various affinities for particular trk receptors, the elimination of NGF, BDNF, and NT-3 has an impact comparable to or more complex than the absence of their most specific high-affinity receptors: trkA, trkB, and trkC, respectively. These complexities include potential NT-3 signaling through trkA and trkB to support some neuronal survival. Third, most types of afferents are dependent on a different combination of neurotrophins and receptors for their survival: reticular and transverse lanceolate afferents are dependent upon NT-3, NGF, and trkA; Ruffini afferents upon BDNF and trkB; longitudinal lanceolate afferents upon NGF, trkA, BDNF, and trkB; and Merkel afferents on NGF, trkA, NT-3, trkC, and p75. NT-4 has no obvious detrimental impact on the mechanoreceptor development in the presence of BDNF. Fourth, NT-4 and BDNF signaling through trkB may suppress Merkel innervation and NT-3 signaling through trkC may suppress Ruffini innervation. Finally, regardless of the neurotrophin/receptor dependency for afferent survival and neurite outgrowth, NT-3 has an impact on the formation of all the sensory endings. In the context of these findings, indications of competitive and suppressive interactions that appear to regulate the balance of innervation density among the various sets of innervation were evident.
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