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The production of cobalt phosphate particles was examined using the forced hydrolysis reaction of Co(NO3)2–pyrophosphate (pp: P2O74−) solutions at 100°C for 18 h. The produced particles were characterized by various physicochemical techniques. No particles were produced at higher concentrations of pp or lower concentrations of Co(NO3)2. Plate-like cobalt pyrophosphate particles were produced at all other concentrations of the aforementioned molecules. The width and length of the large plate-like particles ranged from 654 to 1057 nm and from 293 to 571 nm, respectively, while the sizes of the small plate-like particles were ca. 70 nm in width and 45 nm in length. The thicknesses of the small plate-like particles present in two separate samples were estimated to be 16.8 and 16.3 nm from the TEM images. These values are in fair agreement with the calculated d values of 19.6 and 14.4 nm found using Bragg’s equation at XRD peaks of 2θ = 0.45° and 0.62°. The XRD patterns of the small plate-like particles exhibit two small characteristic peaks for Co2P2O7·2H2O, and the large particles produced peaks that were amorphous (broad bands). The concentrations of cobalt and phosphorus of the assayed particles were lower than the theoretical concentrations estimated from the chemical structure of Co2P2O7·2H2O. These lower values are believed to be caused by the lower crystallinity of the particles. The isotherms of H2O adsorption on the small amorphous plate-like particles were step-like at a relative pressure of 0.1–0.2. However, no step-like behavior was observed for other adsorbed molecules such as N2, CCl4, and CH3OH. The observed steps for the amorphous plate-like particles are explained by the swelling of the particles caused by the H2O molecules. The swelling model was further confirmed by the adsorption–desorption measurement of H2O. The adsorption of H2O molecules onto the small plate-like particles was proven to be a reversible reaction. [ABSTRACT FROM AUTHOR]

Abstract: Aims: The expression of brain-derived neurotrophic factor (BDNF) may be a downstream target of a variety of antidepressant treatments, and selective serotonin reuptake inhibitors (SSRIs) are used clinically for the treatment of depression. BDNF binds to and activates tyrosine kinases receptor (TrkB) to exert its effects. TrkB, after activation by ligands, stimulates phosphoinositide 3-kinase (PI3K). The downstream target of PI3K is Akt-1, a serine-threonine kinase. BDNF has signaling through the PLC-IP3/Ca2+ pathway. Furthermore, the PLC-γ/IP3/Ca2+ pathway is regulated by the sigma-1 receptors. Here, we examined whether fluvoxamine (FLV) activated Akt-1 and increased phosphorylation of Akt-1 via sigma-1 receptor in PC12 cells. Main methods: We examined the effect of the SSRI, FLV and BDNF on the phosphorylation levels of serine-threonine kinase Akt-1 in PC12 cells using immunoblotting techniques. Key findings: Treatment with 10μM and 100μM FLV of PC12 cells stimulated a 2.4- and 3.8-fold maximal increase in Ser473-phosphorylated Akt-1 levels at 40min, respectively. Treatment with 50ng/ml BDNF also stimulated Ser473 -phosphorylated Akt-1 by 2.6-fold with a maximal increase at 5min. In addition, the phosphorylation induced by FLV and BDNF was blocked by LY294002, a selective inhibitor of PI3K. The sigma-1 receptor agonists dehydroepiandrosterone (DHEA)-sulfate also stimulated a 2.1-fold increase in the level of Ser473-phosphorylated Akt-1. Significance: This study demonstrates that fluvoxamine treatment rapidly increased phosphorylation of Akt-1. And BDNF activated Akt-1 phosphorylation by the TrkB/PI3K/Akt-1 pathway. We conclude that the phosphorylation of Akt-1, downstream of PI3K, was the key to their antidepressant effects. [Copyright &y& Elsevier]

Substantial evidence indicates that brain neurons containing and secreting norepinephrine (NE) and corticotrophin-releasing hormone (CRH) are activated during stress. The acoustic startle reflex (ASR) can be enhanced by CRH neuronal activity in the central nucleus of the amygdala. Our previous study demonstrates an augmentation of the footshock-induced ASR (f-ASR) 1 day after chronic variable stress (CVS) for 13 days. In this study, to evaluate a long-term neural plasticity in NE-CRH systems after CVS, we examined f-ASR 1, 8 or 15 days after CVS. The augmented magnitude of the f-ASR 15 day after CVS was potentiated and delayed compared with that 1 day after CVS. The delayed augmentation of f-ASR was inhibited by repeated treatment with desipramine, maprotiline or paroxetine for 14 days after CVS. A single treatment with any antidepressant agent had no influence the f-ASR while a marked inhibition by a single dose of alprazolam, CRH1-receptor antagonist, prazosin and propranolol was observed. The decreased tyrosine hydroxylase activity in the locus coeruleus and the beta-adrenoceptor down-regulation in the amygdaloid complex might be involved in the inhibiton of the delayed augmentation of f-ASR by repeated antidepressant treatment, leading to the possibility that the delayed sensitization of CRH response to stress after CVS might contribute to the biological mechanism underlying the formation of pathological states such as anxiety and depressive disorders.

Corticotropin releasing hormone (CRH)--and norepinephrine (NE) -containing neurons in the brain are activated during stress. We previously reported a decrease in the basal level of CRH immunoreactivity in the central nucleus of the amygdala and the tyrosine hydroxylase immunoreactivity in the locus coeruleus after chronic variable stress (CVS), whereas both responses were augmented by a novel stress (footshock). Since the acoustic startle reflex (ASR) can be enhanced by the CRH neuronal activity in the central nucleus of the amygdala, we examined the influence of footshock on ASR in rats exposed to CVS. The footshock after CVS caused a significant augmentation of ASR compared with the acute footshock. Moreover, the enhanced startle to acute footshock was maximally increased at 6 min and was absent after 40 min, whereas the maximal change of the enhanced startle to footshock after CVS was delayed to 14 min and the significant enhanced startle was found until 180 min. The footshock-enhanced startle after CVS may be related to the augmentation of CRH-NE activity, leading to the possibility that a prolonged CRH hyperactivity to stress might generate a pathophysiology of major depression with a vulnerability to stress.