Unveiling the mechanism of methylcellulose-templated synthesis of Al2O3 microspheres with organic solvents as swelling agents in microchannel.

Herein, we report a systematic investigation of the preparation of large-pore-volume Al2O3 microspheres using a complex synthesis system with methylcellulose (MC) as the template and gelation initiator and organic solvents as the swelling agent and carrier medium under the flow characteristics of a coaxial microchannel. The adsorption of MC micelles on boehmite colloidal nanoparticles (NPs) was proven and determined by interfacial tension measurements, dynamic light scattering, and cryogenic transmission electron microscopy. Isothermal titration calorimetry demonstrated that the adsorption process was caused by nonspecific hydrophobicity; one binding site was involved, and the affinity constant was 1060 M-1. When the MC:NPs mass ratio exceeded 0.1, the template-NP bridged each other to form large aggregates, thereby forming large mesopores and enhancing the gelation speed. Alkanes, alcohols, and amines were applied to further enhance the porosity, and the swelling capacities were investigated experimentally and theoretically. Amines were efficient swelling agents owing to their excellent ability to swell MC micelles and insert into the acid colloid network. The coaxial microchannel was subjected to molding; this process significantly influenced the morphology and textural properties owing to the internal circulation during droplet formation. When trihexylamine with suitable steric hindrance, alkalinity, and polarity was used as the swelling agent, the microspheres exhibited an optimal specific surface area of 403 m2/g and a pore volume of 1.85 cm3/g.

Glycine receptor-mediated inhibition of medial prefrontal cortical pyramidal cells.

Using whole-cell patch clamp recording on medial prefrontal cortical slices of rats aged 17-33 postnatal days, we demonstrated the glycine-induced strychnine-sensitive outward currents. The amplitude of the peak current increased with the concentrations of glycine with an EC50 of 74.7 µM. Application of 1µM strychnine alone to cells caused a slight inward current without blocking the sIPSCs, indicating that GlyRs in the mPFC are activated by an endogenous ligand that can be released tonically. Glycine reversibly depressed firing rate in cells from both layer 6 and layer 3, with significantly greater inhibition on the former than the latter (EC50 12.9 vs 85.6 µM). Glycine hyperpolarized membrane potential in cells of both layer 6 and layer 3 depending on its concentrations, with an IC50 of 99.1 and 207.2 µM, respectively. We propose that GlyRs participate in a novel inhibitory mechanism in mPFC, modulating neuronal activity. This finding further supports an important role of GlyR in cortical function and dysfunction.