Hydrophilic treatment of bulk graphene-like carbon nitride (g-C3N4) for future applications has aroused extensive interest, due to its enhanced specific surface area and unusual electronic properties. Herein, water-dispersible g-C3N4 with a porous structure can be obtained by chemical oxidation of bulk g-C3N4 with K2Cr2O7-H2SO4. Acid oxidation results in the production of hydroxyl and carboxyl groups on its basal plane and the formation of a porous structure of g-C3N4 at the same time. The porous g-C3N4 appears as networks with tens of micrometers in width and possesses a high specific surface area of 235.2 m(2) g(-1). The final concentration of porous g-C3N4 can be up to 3 mg mL(-1). Compared with bulk g-C3N4, the as-obtained porous g-C3N4 exhibits excellent water dispersion stability and shows great superiority in photoinduced charge carrier separation and transfer. The photocatalytic activities of porous g-C3N4 towards degradation of organic pollutants are much higher than those of the bulk due to the larger band gap (by 0.2 eV) and specific surface areas.

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Phosphatidylinositol 3-kinase (PI3K) and its downstream targets, including Akt (also known as protein kinase B, PKB), mammalian target of rapamycin (mTOR), the 70-kDa ribosomal S6 kinase (p70S6k), and the eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1), may play important roles in long-term synaptic plasticity and memory in many brain regions, such as the hippocampus and the amygdala. The present study investigated the role of the PI3K/Akt-mTOR signaling pathway in the medial prefrontal cortex (mPFC), also a crucial neural locus for the control of cognition and emotion. Western blot analysis of mPFC tissues showed an activation of phosphorylation of Akt at the Ser473 residues, mTOR, p70S6k, and 4E-BP1 in response to long-term potentiation (LTP)-inducing high-frequency stimulation (HFS). Infusion of PI3K inhibitors (wortmannin and LY294002) and an mTOR inhibitor (rapamycin) into the mPFC in vivo suppressed HFS-induced LTP as well as the phosphorylation of PI3K/Akt-mTOR signaling pathway. In parallel, these inhibitors interfered with the long-term retention of trace fear memory examined 3 d and 6 d after the trace fear conditioning training, whereas short-term trace fear memory and object recognition memory were kept intact. These results provide evidence of involvement of activation of the PI3K/Akt-mTOR signaling pathway in the mPFC for LTP and long-term retention of trace fear memory.

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