Search

A new phase of Cd(py)4NbOF5 (py = pyridine) (A) is a rare example of a mixed metal oxide fluoride in an ordered linear chain structure. This phase is of particular interest because it is a polymorph of a previously reported Cd(py)4NbOF5 phase (B) that crystallizes in disordered linear chains. The ordered polymorph A contains two distinct Cd2+ sites:  one which is coordinated to the oxide ligands from two [NbOF5]2- units, and another that is coordinated to two trans fluoride ligands. As a result, the structure of polymorph A features nonpolar linear chains with locally ordered [NbOF5]2- anions. This ordering is explained in terms of the inherent electronic differences between oxide and fluoride ligands. The stabilization provided by π-stacking interactions between pyridine ligands on neighboring chains, as well as the effects of reactant stoichiometry on the general structure of the products in the CdO·1/2Nb2O5/(HF)x·py/H2O system, is also discussed. Crystal data for the ordered Cd(py)4NbOF5 polymorph:  monoclinic space group P21/c (No. 14) with a = 14.097(1) Å, b = 16.353(1) Å, c = 10.4380(9) Å, β = 95.569(2)°, and Z = 4. [ABSTRACT FROM AUTHOR]

To identify brain regions, cell types, or both that generate abnormal electrical discharge in tuberous sclerosis complex (TSC). Here we examined excitatory and inhibitory synaptic currents in human tissue samples obtained from a TSC patient with no discernible cortical tubers and acute neocortical brain slices from a mouse featuring synapsin‐driven conditional deletion of a TSC1 gene. These studies were designed to assess whether TSC gene inactivation alters excitability.We used visualized patch‐clamp (human and mouse) and extracellular field (mouse) recordings. Additional mice were processed for immunohistochemistry or Western blot analysis.Detailed anatomic studies in brain tissue sections from synapsin‐TSC1 conditional knock‐out mice failed to uncover gross anatomic defects, loss of lamination, or frank tuber formation. However, regions of abnormal and potentially activated neocortex were shown using antibodies to nonphosphorylated neurofilaments (SMI‐311) and immediate early genes (c‐Fos). Extracellular recordings from neocortical slices, examining synaptic activity in these regions, demonstrated clear differences in excitability between conditional knock‐out and age‐matched control mice. Whole‐cell patch‐clamp recordings demonstrated excitatory synaptic currents with strikingly long duration and epileptiform discharge patterns, similar to waveforms observed in our human tissue samples. These events were 1‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptor mediated and were most prominent in neocortex. Normal‐appearing inhibitory postsynaptic currents (human) and intrinsic neuronal firing patterns (mouse) were also recorded.This combination of human and mouse tissue studies suggests, for the first time, that synaptic excitation is altered in a direction that favors seizure generation in TSC brain tissue regardless of cortical tubers. Ann Neurol 2007 [ABSTRACT FROM AUTHOR]