Porous TiO 2 films decorated with Bi 2 O 3 nanoparticles are fabricated via alkalihydrothermal of titanium (Ti) plate by varying the reaction time. The amorphous TiO 2 is transformed into anatase after annealing the films at 500°C in air. The p-type Bi 2 O 3 nanoparticles are successfully assembled on the surface of porous n-type TiO 2 films through the ultrasonic-assisted successive ionic layer adsorption and reaction (SILAR) technique to form Bi 2 O 3 /TiO 2 nanostructure by the two cycles. The obtained Bi 2 O 3 /TiO 2 films are consisted of a well-ordered and uniform porous structure with an average pore diameter of about 100-200 nm containing homogeneously dispersed Bi 2 O 3 nanoparticles of~5 nm diameter. Moreover, the resultant composites present excellent photocatalytic performance toward methyl blue (MB) degradation under UV and visible light irradiation, which could be mainly ascribed to the enhanced light adsorption capacity of unique composite structure and the formation of p-n heterojunctions in the porous Bi 2 O 3 /TiO 2 films. This research is helpful to design and construct the highly efficient heterogeneous semiconductor photocatalysts.

Cooperating mercapto groups with tacrine in a single molecular, novel multifunctional compounds have been designed and synthesized. These mercapto-tacrine derivatives displayed a synergistic pharmacological profile of long-term potentiation enhancement, cholinesterase inhibition, neuroprotection, and less hepatotoxicity, emerging as promising molecules for the therapy of age-related neurodegenerative diseases.

As an endogenous gaseous molecule, hydrogen sulfide (H 2 S) has attracted extensive attention because of its multiple biological effects. However, the effect of H 2 S on amygdalamediated emotional memory has not been elucidated. Here, by employing Pavlovian fear conditioning, an animal model widely used to explore the neural substrates of emotion, we determined whether H 2 S could regulate emotional memory. It was shown that the H 2 S levels in the amygdala of rats were significantly elevated after cued fear conditioning. Both intraamygdala and systemic administrations of H 2 S markedly enhanced amygdala-dependent cued fear memory in rats. Moreover, it was found that H 2 S selectively increased the surface expression and currents of NMDA-type glutamate receptor subunit 2B (GluN2B)-containing NMDA receptors (NMDARs) in lateral amygdala of rats, whereas blockade of GluN2B-containing NMDARs in lateral amygdala eliminated the effects of H 2 S to enhance amygdalar long-term potentiation and cued fear memory. These results demonstrate that H 2 S can regulate amygdala-dependent emotional memory by promoting the function of GluN2B-containing NMDARs in amygdala, suggesting that H 2 S-associated signaling may hold potential as a new target for the treatment of emotional disorders.

BACKGROUND AND PURPOSEPosttraumatic stress disorder (PTSD) is a mental disorder with enhanced retention of fear memory and has profound impact on quality of life for millions of people worldwide. The β-adrenoceptor antagonist propranolol has been used in preclinical and clinical studies for the treatment of PTSD, but the mechanisms underlying its potential efficacy on fear memory retention remain to be elucidated. EXPERIMENTAL APPROACHWe investigated the action of propranolol on the retention of conditioned fear memory, the surface expression of glutamate receptor GluA1 subunits of AMPA receptors and synaptic adaptation in the lateral amygdala (LA) of rats. KEY RESULTSPropranolol attenuated reactivation-induced strengthening of fear retention while reducing enhanced surface expression of GluA1 subunits and restoring the impaired long-term depression in LA. These effects of propranolol were mediated by antagonizing reactivation-induced enhancement of adrenergic signalling, which activates PKA and calcium/calmodulin-dependent protein kinase II and then regulates the trafficking of AMPA receptors via phosphorylation of GluA1 subunits at the C-terminus. Both i.p. injection and intra-amygdala infusion of propranolol attenuated reactivation-induced enhancement of fear retention. CONCLUSIONS AND IMPLICATIONSReactivation strengthens fear retention by increasing the level of noradrenaline and promotes the surface expression of GluA1 subunits and the excitatory synaptic transmission in LA. These findings uncover one mechanism underlying the efficiency of propranolol on retention of fear memories and suggest that β-adrenoceptor antagonists, which act centrally, may be more suitable for the treatment of PTSD. Abbreviations

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