The MOF material NH 2 -MIL-125(Ti) was synthesized through the solvothermal method, and the morphology can be controlled by simply modulating the concentration of the reactants during crystallization, which ranges from circular plate through tetragon to octahedron. All samples were characterized by SEM, XRD, FT-IR, UV Raman spectra, TGA, Ar adsorption/desorption and UV-vis spectra.In situ XRD results show that this Ti-incorporated MOF is highly thermostable until 290 °C. It is interesting to find that the light response of NH 2 -MIL-125(Ti) crystals is closely related to their morphology, and the absorption edges of different morphologies range from 480 nm to 533 nm with band gaps of 2.6 to 2.3 eV, making them potential candidates for photocatalytic applications.

Two receptors for vasopressin (Avp) are expressed in the brain, the Avp 1a receptor (Avpr1a) and the Avp 1b receptor (Avpr1b). To investigate the role of Avpr1a in behaviors in mice more extensively, we generated a line of mice lacking a functional Avpr1a (knockout, Avpr1a 2/2 ). We first performed a baseline phenotypic screen of the Avpr1a knockouts followed by a more detailed analysis of their circadian rhythms and olfactory function. When free-running in constant darkness, the Avpr1a 2/2 mice have a longer circadian tau than the wild types. There are also subtle olfactory deficits in Avpr1a 2/2 mice as measured in an olfactory habituation/dishabituation test and in the discrimination of female urine from male urine using an operant testing paradigm. An extensive body of research has shown that manipulation of the Avpr1a alters behavior, including aggression and social recognition. Therefore, we expected profound behavioral deficits in mice lacking the Avpr1a gene. Contrary to our expectations, social aggression, anxiety-like behavior and social recognition are unaffected in this line of Avpr1a knockout mice. These data suggest either that the Avpr1a is not as critical as we thought for social behavior in mice or, more likely, that the neural circuitry underlying aggression and other social behaviors compensates for the life-long loss of the Avpr1a. However, the olfactory deficits observed in the Avpr1a 2/2 mice suggest that Avp and Avpr1a drugs may affect behavior, in part, by modulation of chemosensory systems.

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