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The selective antagonist at the CRF1 receptor, SSR125543, has been shown to produce anxiolytic-like effects in a number of animal models. The aim of the present study was to verify whether these effects are mediated by an action on the hypothalamic pituitary adrenal (HPA) axis. SSR125543 effects were evaluated in a mouse model of post-traumatic stress disorder. Animals received two unavoidable electric foot-shocks (1.5 mA/2 s). Two weeks later they were placed in the shock context and fecal and plasma corticosterone levels were measured by enzyme-immunoassay. Their cognitive performances were evaluated using the object recognition task following administration of SSR125543 at 3, 10 and 30 mg/kg or paroxetine at 20 mg/kg (i.p.), used as positive control. To assess the involvement of the HPA axis in the drug effects, a separate group of animals was subjected to the same procedure and drug regimen, but was treated with dexamethasone to blunt the HPA axis. Stressed mice had higher levels of corticosterone following re-exposure to the context and displayed impaired cognitive performance as compared to control animals. Corticosterone levels were normalized in stressed mice by SSR125543 and the cognitive deficit was significantly attenuated by SSR125543 and paroxetine, whether the HPA axis was blunted or not. These findings confirm that SSR125543 is able to attenuate the deleterious effects of stressful exposure. Importantly, the observation that these effects were still present in dexamethasone-treated mice indicates that this action does not necessarily involve pituitary-adrenal axis blockade, thereby suggesting that extra-pituitary CRF1 receptors may play a role in these effects.

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The experience of traumatic stress often leads to long-lasting alteration in sleep quality and behavior. The objective of the present experiment was to investigate the short- and long-term effects of acute inescapable stress (i.e. two electric foot-shocks of 1.5 mA; 2s) on sleep/wakefulness parameters and behavior in Swiss mice using electroencephalographic (EEG) analysis. Baseline EEG recording was performed in the home cage for 6h prior to the application of the foot-shocks in the presence of an object (i.e. a plastic prism). One, 7, 14 or 21 days later, a second 6h EEG recording session was performed after mice had been exposed or not to the same object for 5 min in their home cage. Results showed that at day 1, 7, 14 and 21 post-stress, shocked mice displayed sleep fragmentation as shown by an increase in the number of sleep episodes, regardless the presence of the object or not. In animals exposed to the object, the total duration of wakefulness over 6h was significantly increased at days 7, 14 and 21 post-stress, and rapid eye movement (REM) sleep was significantly decreased at day 14 post-shock. Moreover, in the behavioral experiment, conditioned avoidance to a shock-paired object, which appeared as soon as 24h after shock application, turned into generalized avoidance towards an unknown object 21 days after stress. These findings demonstrate that an acute inescapable stress exposure may cause long-lasting alterations in sleep patterns and behavior. Such modifications may be reminiscent of the profound changes observed in patients suffering from post-traumatic stress disorder.

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This paper outlines the basic events that occur when a semiconductor, in contact with aerated liquid water containing low concentrations of pollutants, is photoexcited. First, the factors favouring this recombination of photoproduced charges are recalled, and the difficulties in decreasing the recombination are underlined. Second, the formation and identification of the species resulting from charge transfer with O2, H2O and pollutants are presented. Third, the reactions involving these species are considered, and methods for assessing their respective importance are critically reviewed. Fourth, on the basis of the view that the photocatalyst surface is covered by tightly bound water layers which hinder the adsorption of many organic pollutants, the hypothesis according to which primary photocatalytic events can take place within the near-surface solution layers is discussed.

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The aim of this study was to assess in a vineyard the effect of purifying by solar photocatalysis the title rinse waters (currently most often rejected) in terms of efficacy and on-site practicality for the wine grower. The on-site, self-functioning, solar purifying unit included a corrugated-steel inclined plate of area S = 1 m2 onto which a TiO2-coated thin material had been slightly pressed, a tank, and an aquarium-type pump powered by a photovoltaic panel (appropriate for isolated locations). For a vineyard of area A = 0.15 km2, the rinse water (about 90 L) corresponding to each of four typical vine treatments in summer was analysed (major pesticides for each treatment, TOC, Microtox test and, in one case, BOD5) by independent laboratories, before and after purification for 8 days. The S/A ratio tested was found insufficient even if the photocatalytic treatment markedly improved the quality of the rinse waters. From the relatively low final organic content reached in one case, it is calculated that a three-time higher S/A ratio might suffice, but new trials are necessary to determine whether it is valid for other typical cases. Inferred contribution of inorganic ions to the post-photocatalytic treatment toxicity points to the need for an additional detoxification. These field experiments have also demonstrated that the purifying prototype is robust, and easy to install and use on site by the wine grower.

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The photocatalytic removal rates r of dichloroacetic acid (DCAA), 4-chlorobenzoic acid (4-CBA) and 4-chlorophenol (4-CP) in water were compared for TiO2 samples used either as a powder or as a coating on a fiber glass tissue, SiO2 being the binder. From SEM-EDX measurements it was deduced that SiO2 prevails over TiO2 in the coating top layers and 18O2-Ti16O2 isotopic exchange showed that the accessibility of O2 to TiO2 was markedly reduced when TiO2 was thus coated. The unfavorable effect of the restricted TiO2 accessibility on r was drastic for DCAA, much less pronounced for 4-CBA, and still smaller for 4-CP. It is inferred that DCAA can be attacked only when it directly interacts with TiO2, whereas 4-CP can also react within the near-TiO2 surface water layers. The 4-CBA intermediate behavior is in line with the structural similarities of 4-CBA with DCAA and 4-CP.

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Solid-phase micro-extraction has been used for identifying, quantifying and following the evolution of intermediate products of octanol degradation by two advanced oxidation treatments (AOTs), photocatalytic and ultrasound processes, inducing mainly the same active species. Headspace extraction enabled direct extraction of the organic compounds in a heterogeneous process like photocatalysis. The presence of a solid does not affect the extraction percentage of alkanes, alkenes and aldehydes while alcohols and carboxylic acids are not completely extracted if the extraction time is too short. To extract C3-C8 alkanes, alkenes and aldehydes a Carboxen/PDMS fiber and an extraction time of 25 min are used. The presence of alcohol and carboxylic acids requires the use of the presence of salt under acidic conditions, a longer extraction time and a polyacrylate fiber (PA), having a polar fiber. The in situ derivatization--pyrenyldiazomethane on a PA fiber--increases the carboxylic acid extraction containing smaller hydrocarboned chain while diazomethane derivatization is not as efficient due to its volatility. Whatever be the treatment, photocatalysis or ultrasound processes, aldehydes are the main intermediate products, which is not surprising since the same oxidation species (HO2(o), O2(o-), OH(o)) are formed. Alkanes and alkenes are also detected in both processes; however, alkane formation is more important in photocatalysis while alkenes are formed in higher amounts by ultrasound. Moreover, the presence of carboxylic acids in more important amounts by ultrasound than by photocatalysis is attributed to the presence of holes (h+) in photocatalysis which induces photo-Kolbe degradation. The sonochemical formation of small-chained dienes and alkynes is probably due to pyrolysis of hydrophobic compounds in cavitation bubbles.

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TiO2 photocatalysis and ultrasound are advanced oxidation processes for water treatment. Our study aimed at showing, via the purposely chosen title compounds, that these techniques can be complementary. For C6H5COCF3 (PTMK), the photocatalytic removal rate was higher than the ultrasonic (515 kHz) removal rate in the presence of TiO2 in the dark, whereas it was the opposite for octan-1-ol under the conditions employed. Simultaneous UV and ultrasound irradiation of the TiO2 suspension led, for PTMK, to a removal rate about equal to the sum of the removal rates observed for separate irradiations, and decreased by a factor of approximately 20% for octan- 1 -ol as if the photocatalytic degradation was suppressed by the dominant distribution of octan-1-ol to the cavitation bubbles. This distribution was substantiated by the large detrimental effect of octan- 1-ol on the PTMK ultrasonic removal rate. The concurrent use of both techniques allowed a faster removal of both pollutants in binary mixtures. The amount of CF3COOH from PTMK was approximately eight times lower in sonicated, than in UV-irradiated, TiO2 suspensions. Several intermediate products showed the occurrence of chemical transformations occurring in and/or on the cavitation bubbles. COD decline and CO2 formation were initially higher for ultrasonic than for photocatalytic treatment. However, complete mineralization (except for CF3COOH) was achieved more rapidly by photocatalysis and even more rapidly by simultaneous use of both techniques.

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The anti-inflammatory effect of mizolastine (CAS 108612-45-9, SL85.0324-00), a new non-sedative histamine H1-receptor antagonist, was assessed in comparison to loratadine, terfenadine and pyrilamine. Intraplantar injection of arachidonic acid (AA) into the rat paw was followed by a rapid and sustained (> or = 4h) inflammatory oedema. Mizolastine (0.1 to 10 mg/ kg p.o.) inhibited in a dose-dependent manner the time course of the AA-induced paw inflammation as from the dose of 0.1 mg/kg p.o. This effect was maintained for at least the 4 h of observation (-44% at 0.3 mg/kg p.o.) suggesting a long lasting action of mizolastine. Although with higher maximal effect, a similar time course of response was observed with dexamethasone at 0.1 mg/kg p.o. In contrast, at anti-histamine, doses, the histamine H1-receptor antagonists terfenadine (1 to 30 mg/kg p.o.), loratadine (10 mg/kg p.o.), and pyrilamine (10 mg/kg p.o.) failed to inhibit significantly the inflammatory action of AA. Moreover, under conditions of H1-receptors blockade (e.g. when co-administered with pyrilamine or loratadine (10 mg/kg p.o.), the inhibition by mizolastine (0.3 mg/kg) of AA-induced inflammation was unchanged. This suggests that the anti-inflammatory effect of mizolastine was unrelated to its histamine H1-receptor antagonist properties. It is proposed that a primary effect on the lipoxygenase pathway may contribute to this action of mizolastine. This is based on the observations that mizolastine inhibits 5-lipoxygenase activity in vitro. Furthermore, a high dose of mizolastine (50 mg/kg) did not affect the inflammatory response to carrageenin which is mediated by the cyclooxygenase pathway. Together, these data indicate that mizolastine is orally effective in this animal model for cutaneous inflammation. Combined with its blockade of histamine H1-receptors, this property may contribute to its possible use in allergic inflammation or other inflammatory states.

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In the present study the effect of mizolastine (CAS 108612-45-9, SL85.0324-00) a novel potent histamine H1-receptor antagonist, on 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis, a rat model of inflammatory bowel disease, was investigated to determine whether mizolastine has anti-inflammatory properties. Treatment with TNBS resulted in increased nociception in response to rectal balloon distension and caused intestinal damage, tissue oedema and inflammation. Oral mizolastine (0.03-3.00 mg/kg given 1 h before and once daily for 3 days after TNBS treatment) significantly (p < 0.05) reduced nociception (49% at 0.3 mg/kg), gross intestinal damage (78% at 3.0 mg/kg), histological damage (54% at 3.0 mg/kg), intestinal tissue weight (69% at 3.0 mg/kg) and myeloperoxidase activity (66% at 3.0 mg/kg). In contrast, the H1-receptor antagonist terfenadine tested under the same experimental conditions at 3-30 mg/kg was without significant effect. It is concluded that, in addition to its antiallergic properties, mizolastine possesses anti-inflammatory actions that may not be related to its H1-receptor blocking properties, reducing sensory afferent hypersensitivity, damage and neutrophil infiltration observed during colitis.

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Recent advances in the psychopharmacology of GABA synapses are reviewed. The usefulness of GABA mimetics in tardive dyskinesia and epilepsy has been confirmed, as has a dysfunction of GABA synapses in the etiopathology of these conditions. The antidepressant profile of GABA agonists in animal models for depression has been extended. The role of GABA receptors in the mechanism of action of antidepressants has been further delineated, with a parallelism occurring between the behavioral and biochemical response to antidepressant drug treatment in different animal models of depression.

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Recently, sufficient evidence has accumulated to suggest that a central GABAergic dysfunction may be primarily related to the physiopathology of affective disorders and that antidepressant mechanisms have an intrinsic GABAergic component. In depressed patients GABA levels are reported to be low in the cerebral spinal fluid and plasma, and GABA synthesis is decreased in some brain areas, including the frontal cortex. GABA mimetics exhibit antidepressant-like actions in behavioral models in the olfactory bulbectomized rat and in the learned helplessness paradigm. In the olfactory bulbectomized rat, GABA B receptors are down regulated in the frontal cortex and in the learned helplessness paradigm, GABA release is diminished in the hippocampus. These decreases are reversed by antidepressants in parallel with their behavioral activities. In this study, data obtained indicate that in the learned helplessness paradigm, GABA B receptors are decreased in the frontal cortex and this decrease is reversed by imipramine and desipramine (16 mg/kg/day) in animals which are considered to be 'responders' to antidepressant treatments.

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Little is known about the implication of central GABAergic neurons. However, there is evidence suggesting a growing importance of GABAergic function in the action of antidepressants. Since streptozotocin (STZ)-diabetic rats have been shown to be resistant to the action of various antidepressants, we were interested in evaluating the density of GABAergic receptor binding sites in the cortex of STZ-diabetic rats on day 15 and day 30 of diabetes. A specific and marked decrease in GABA B receptor density was observed with no change in GABA A. Although no clear relationship could be demonstrated, it may be suggested that a central GABAergic dysfunction of diabetic rats may contribute to explain their resistance to antidepressants.

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