Study of Balance Equations for Hot-Electron Transport in an Arbitrary Energy Band (III)

By choosing an electron gas resting instead of drifting in the laboratory coordinate system as the initial state, the first order perturbation calculation of the previous paper (Phys. Stat. Sol. (b) 198, 785(1996)) is revised and extended to include the high order field corrections in the expression for the frictional forces and the energy transfer rates. The final expressions are formally the same as those in first order in the electric field, but the distribution functions of electrons appearing in them are defined by different expressions. The problems relative to the distribution function are discussed in detail and a new closed expression for the distribution function is obtained. The nonlinear impurity-limited resistance of a strong degenerate electron gas is computed numerically. The result calculated by using the new expression for the distribution function is quite different from that using the displaced Fermi function when the electric field is sufficiently high.Comment: 15 pages with 3 PS figures, RevTeX, to be published in Physica Status Solidi (b

Characterisation of anatomical and functional deficits in a mouse model of Rett Syndrome

Rett syndrome (RTT), a disorder caused almost exclusively by mutations in the X-linked gene, MECP2, has a clinical phenotype thought to be primarily of neurological origin. Disruption of Mecp2 in mice results in a prominent RTT-like phenotype and Mecp2 knock-out animal models provide an excellent platform for investigating the role of MeCP2 in the brain development. In this thesis, I used the Mecp2-stop mouse model to address the effects of MeCP2 deficiency in the central nervous system. First, I assessed the genotype-phenotype relationship at the level of the whole organism by detailed temporal mapping of the RTT-like neurological signs. I also addressed the genotype-phenotype relationship at the level of neuronal networks by assessing alterations in neuronal (cortical) density including potential alterations across morphologically discrete cell subtypes. Finally, I also investigated the genotype-phenotype relationship at the level of the synapse by assessing RTT-related changed in synaptic plasticity. Whole organism phenotyping using observational scoring revealed the male hemizygous Mecp2-mutant mice (Mecp2stop/y) to show an early (from ~5 weeks) and aggressive onset of signs including locomotor and other general features. Correlated studies at the level of the synapse revealed the severity of gross organismal pathology to mirror a progressive decline in both short- and long-term forms of synaptic plasticity as measured in the CA1 region of the hippocampus. Specifically, extracellular field recordings in acute hippocampal slices from strongly symptomatic Mecp2-stop mice showed long-term plasticity (LTP) at the Schaffer-collateral-to-CA1 pyramidal synapse to be 40.2 ± 1.6 % of age-matched wild-type littermate controls. In addition, putative presynaptic short-term forms of plasticity (post-tetanic potentiation (PTP) and paired-pulse facilitation (PPF)) were also decreased in the Mecp2-stop hippocampus (45 ± 18.8 % and 78 ± 0.1 % of wild type for PTP and PPF respectively; all p<0.05). Moreover, the impairment in LTP was associated with symptom severity score whereby mice with a more ‘severe’ symptom score showed a more profound deficit in LTP. Refined axon stimulation protocols revealed evidence of pronounced LTP saturation in symptomatic Mecp2stop/y mice, suggesting an LTP ‘ceiling’ effect. I therefore assessed the action of the weak NMDA receptor blocker memantine, shown previously to reverse LTP saturation-related LTP deficits, in the hippocampus of control and Mecp2-stop mice. Application of memantine (1μM), resulted in substantial reversal of short-term plasticity deficits in the Mecp2-stop samples, without affecting plasticity in wild-type mice. However, systemic administration of memantine (30mg/Kg) in vivo did not have any observable effect on RTT-like phenotype at the organismal level including symptom onset, progression and survival. Utilising immunohistochemistry (NeuN) and histological staining (DAPI) to quantify cell density in layer five of the somatosensory cortex, I demonstrated that the symptomatic Mecp2-stop mouse had a higher cortical cell density compared to wild-type controls (1.28 times of whole cortical cell density and 1.41 times of neuronal cell density). Detailed analyses of distinct neuronal subpopulations (parvalbumin-, somatostatin-, calretinin- and calbindin-immunopositive cells) showed that calretinin (CR)- and somatostatin (SOM)- immunopositive cells had a lower cell density in Mecp2-stop mouse somatosensory cortex. However, the distribution patterns of different neuronal subtypes (using the same markers) in Mecp2-stop hippocampus were preserved and were grossly similar to those of WT brains. In summary, in this thesis, I demonstrated that the cell densities of CR- and SOM- positive neurons were altered in the somatosensory cortex in symptomatic Mecp2-stop mice. At the synaptic functional level, I showed both short-term and long-term plasticity deficits in the hippocampus of Mecp2-stop brains. Memantine, a clinically widely-used Alzheimer drug, partially restored the synaptic plasticity deficits in vitro. These data together supported that deficits in specific neuronal populations and progressive functional synaptic impairment may be key features in the RTT brain and also demonstrated the potential for the pharmacological restoration of synaptic plasticity function

μ-Cyanido-1:2κ2 N:C-tricyanido-2κ3 C-(rac-5,5,7,12,12,14-hexa­methyl-1,4,8,11-tetra­aza­cyclo­tetra­decane-1κ4 N,N′,N′′,N′′′)dinickel(II) N,N-di­methyl­formamide monosolvate hemi­hydrate

The two NiII atoms in the title complex, [Ni2(CN)4(C16H36N4)]·C3H7NO·0.5H2O, are bridged by a cyanide ion. The macrocycle folds around one NiII atom, which is five-coordinated in an NiN5 square-pyramidal geometry. The other NiII atom is surrounded by the cyanide ions in an NiN4 square-planar geometry. The dimethyl­formamide solvent mol­ecule is disordered over two positions in a 0.62 (1):0.38 (1) ratio and the water mol­ecule is disordered about a center of inversion. The dinuclear mol­ecule and solvent mol­ecules are linked by N—H⋯O, N–H⋯N and O—H⋯O hydrogen bonds, forming a three-dimensional network