Electron correlation and spin-orbit coupling effects in US3 and USe3

A systematic density functional theory (DFT)+U study is conducted to investigate the electron correlation and spin-orbit coupling (SOC) effects in US3 and USe3. Our calculations reveal that inclusion of the U term is essential to get energy band gaps for them, indicating the strong correlation effects for uranium 5f electrons. Taking consideration of the SOC effect results in small reduction on the electronic band gaps of US3 and USe3, but largely changes the energy band shapes around the Fermi energy. As a result, US3 has a direct band gap while USe3 has an indirect one. Our calculations predict that both US3 and USe3 are antiferromagnetic insulators, in agreement with corresponding experimental results. Based on our DFT+U calculations, we systematically present the ground-state electronic, mechanical, and Raman properties for US3 and USe3.Comment: 6 pages, 6 figure

Modulation of the slow/common gating of CLC channels by intracellular cadmium.

Members of the CLC family of Cl(-) channels and transporters are homodimeric integral membrane proteins. Two gating mechanisms control the opening and closing of Cl(-) channels in this family: fast gating, which regulates opening and closing of the individual pores in each subunit, and slow (or common) gating, which simultaneously controls gating of both subunits. Here, we found that intracellularly applied Cd(2+) reduces the current of CLC-0 because of its inhibition on the slow gating. We identified CLC-0 residues C229 and H231, located at the intracellular end of the transmembrane domain near the dimer interface, as the Cd(2+)-coordinating residues. The inhibition of the current of CLC-0 by Cd(2+) was greatly enhanced by mutation of I225W and V490W at the dimer interface. Biochemical experiments revealed that formation of a disulfide bond within this Cd(2+)-binding site is also affected by mutation of I225W and V490W, indicating that these two mutations alter the structure of the Cd(2+)-binding site. Kinetic studies showed that Cd(2+) inhibition appears to be state dependent, suggesting that structural rearrangements may occur in the CLC dimer interface during Cd(2+) modulation. Mutations of I290 and I556 of CLC-1, which correspond to I225 and V490 of CLC-0, respectively, have been shown previously to cause malfunction of CLC-1 Cl(-) channel by altering the common gating. Our experimental results suggest that mutations of the corresponding residues in CLC-0 change the subunit interaction and alter the slow gating of CLC-0. The effect of these mutations on modulations of slow gating of CLC channels by intracellular Cd(2+) likely depends on their alteration of subunit interactions

Slow in Motion but Smart in Learning and Memory: Behavioral Changes in Adult NR3A Knockout Mice

The expression of NMDA receptor subunit NR3A is high in the neonatal brain but low in adults. However, its functional role in the adult brain is obscure. Using wild-type (WT) and NR3A knockout (KO) mice, we show here that NR3A plays imperative roles in multiple behavioral functions in adults. NR3A deletion produced a slow locomotor phenotype with enhanced memory capacities. Hippocampal slices from juvenile and adult NR3A KO mice showed greater long-term potentiation (LTP) compared to WT slices. NR3A deletion resulted in increased expression and phosphorylation of calmodulin-dependent kinase II (CaMKII). CaMKII inhibition abrogated the enhanced LTP in NR3A KO slices. NR3A KO mice were also more sensitive to acute and chronic pain. These data reveal for the first time that NR3A, despite its low expression, plays several critical roles in behavioral activities in adults and may be a therapeutic target for modulating behaviors under normal and pathological conditions