The UV photoproduction of a hydrophilic TiO 2 (110)(1×1) surface has been investigated in a pressurized ultrahigh vacuum apparatus under controlled conditions of hydrocarbon concentration in oxygen gas at 1 atm pressure. Water droplet contact angles have been measured continuously as the droplet is exposed to UV irradiation, yielding the first observations of a sudden wetting process during irradiation. Using hexane as a model hydrocarbon, it is found that when low partial pressures of hexane are present, the sudden onset of surface wetting occurs during UV irradiation after an induction period under photooxidation conditions. The induction period to reach the critical condition for sudden wetting increases when the partial pressure (and equilibrium surface coverage) of hexane is increased. These results indicate that the removal of adsorbed hydrocarbons by photooxidation is the critical factor leading to the UV-induced hydrophilicity phenomenon on TiO 2 . The phenomenon does not occur in the absence of O 2 gas. A concept concerned with kinetic screening of the TiO 2 -H 2 O interface from O 2 by water droplets is presented to explain the observation of sudden wetting in our experiments, compared to gradual wetting which is observed following UV irradiation in all other experiments reported in the literature. Complementary infrared spectroscopy measurements of the effect of UV irradiation in an O 2 atmosphere on adsorbed Ti-OH groups and on adsorbed H 2 O on the surface of a high-area TiO 2 powder show that no spectroscopic changes occur. This indicates that UV-induced changes in the -OH coverage or the nature of -OH bonding to TiO 2 , as suggested by others, cannot be used to explain the photoinduced hydrophilicity effect.
It was previously shown that a moderate dose of cocaine (10 mg/kg i.p.) produces a pattern in the EEG power spectrum which indicates a preferential activation of dopamine D1-like receptors, namely a decrease of power in most of the frequency bands. In contrast, a large dose of cocaine (30 mg/kg i.p.) produces a decrease of power in most of the frequency bands as well, but a selective increase in the alpha-1 band, characteristic for an additional activation of dopamine D2-like receptors. In the present experiments, it was studied in rats, if in the course of sensitization, a shift from D1-like to additional D2-like receptor activation will occur or not. For this study, the animals were treated 10 times with cocaine (either 10 or 20 mg/kg) and, after a drug free interval of 4 days, tested with the same dose administered previously. Acute administration of 10 mg/kg of cocaine increased the locomotor activity slightly and its effect tended to be enhanced after repeated administration. Twenty mg/kg cocaine increased the locomotor activity more than the 10 mg/kg dose and its effect was significantly enhanced after repeated treatment. In addition, it was shown that the dose of 10 mg/kg of cocaine which activates D1- but not D2-like receptors is sufficient to elicit conditioned place preference. Ten mg/kg of cocaine produced a decrease of power in most of the frequency bands and this effect was slightly more pronounced after repeated treatment. Twenty mg/kg of cocaine acutely also produced a decrease in power in most of the frequency bands, but did not decrease the power in the alpha-1 band, being just at the threshold of activating D2-like receptors as well. Repeated administration led to a significant increase in power in the alpha-1 band and a less pronounced one in the alpha-2 band. This observation demonstrates that sensitization to cocaine can be manifest in the EEG and that after a certain dosage, a shift from an activation of D1-like dopamine receptors to an additional activation of D2-like receptors becomes obvious.
After repeated administration of cocaine or d-amphetamine, a sensitization to their behavioural effects is frequently observed instead of a tolerance. In a previous study, it was shown that a moderate dose of d-amphetamine produced a pattern of EEG power spectrum which indicated a selective activation of D1-like dopamine receptors, whereas a larger dose induced a selective increase of power in the alpha-1 frequency band and, to a lesser degree, in the alpha-2 band, suggesting an additional activation of D2-like receptors. Furthermore, it was recently found that under a certain dosage and schedule, cocaine could produce a shift from a D1-characteristic to a D2-like EEG pattern. It was now studied, if the same is true for d-amphetamine. This drug was administered on 4 subsequent days (0.6 mg/kg i.p.); after an interval of 3 days, the same dose was administered. After repeated, but not a single administration, increases in the power of the alpha-1 and alpha-2 frequency bands were observed, suggesting a shift from activation of D1-like to additional activation of D2-like receptors. This shift was accompanied by a slight enhancement in stereotyped behaviour (sniffing). After a lower dose (0.2 mg/kg), no EEG effect could be observed, neither after a single nor after repeated administration.
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