For the quantum wire stacks with different InAs layer thicknesses and a separation of 8 nm, double peak photoluminescence spectra were observed in the sample with 4 ML of InAs, and a main peak with a long wavelength component was obtained from the sample with 3 ML of InAs. Only a single peak was detectable for the InAs layer thicknesses
of 5 and 7 ML. The optical emission features were studied via temperature and excitation laser power dependent photoluminescence. Based on the photoluminescence and transmission electron microscopy observations, photoluminescence spectral features can be attributed to a bi-modal height distribution in certain samples. In order to extend the optical emission to room temperature, the sample with 5 ML of InAs and an 8 nm spacer layer was subjected to post-growth Selleckchem JNK-IN-8 rapid thermal annealing at different temperatures. The emission
wavelength was tunable from 1.63 to 1.72 mu m at room temperature. (C) 2011 American Institute of Physics. [doi:10.1063/1.3598082]“
“Nicotinic drugs have been proposed as putative drugs to treat Parkinson’s disease (PD). In this study, we investigated whether nicotine can sensitize parkinsonian animals to the effect of dopaminergic drugs. Testing this hypothesis is important because nicotine has been shown to present neuroprotective and acute symptomatic effects on PD, but few studies have addressed the question of whether it may induce long-lasting effects on dopamine neurotransmission. We tested this hypothesis in the 6-hydroxydopamine (6-OHDA) rat model of PD. A pretreatment of these rats with 0.1-1.0 mg/kg nicotine induced a dose-dependent sensitization of the turning behavior Staurosporine ic50 when the animals were challenged with the dopamine receptor agonist apomorphine 24 h later. In agreement with previous studies, while apomorphine induced contraversive turns, nicotine, as well as amphetamine, induced ipsiversive turns in the 6-OHDA rats. This result suggests that, like amphetamine, nicotine induces turning selleck kinase inhibitor behavior by promoting release of
dopamine in the non-lesioned striatum of the rats. However, it is unlikely that the release of dopamine may also explain the nicotine-induced sensitization of turning behavior. First, the dopamine amount that could be released in the lesioned hemi-striatum by the nicotine pretreatment was minimum-less than 3%, as detected by HPLC-EC. Second, a pretreatment with amphetamine did not induce this behavioral sensitization. A pretreatment with apomorphine-induced sensitization, but it was minimal when compared to that induced by nicotine. Therefore, it is unlikely that the sensitization of the turning behavior induced by nicotine was consequent of the release of dopamine. However, the expression of such sensitization seems to depend on the activation of dopaminergic receptors, since it was seen when the nicotine-sensitized animals were challenged with apomorphine, but not with a second nicotine challenge.