Evaluation of the In desorption during the capped process in diluted nitride In(Ga)As quantum dots

Diluted nitride self-assembled In(Ga)AsN quantum dots (QDs) grown on GaAs substrates are potential candidates to emit in the windows of maximum transmittance for optical fibres (1.3-1.55 μm). In this paper, we analyse the effect of nitrogen addition on the indium desorption occurring during the capping process of InxGa1−xAs QDs (x = l and 0.7). The samples have been grown by molecular beam epitaxy and studied through transmission electron microscopy (TEM) and photoluminescence techniques. The composition distribution inside the dots was determined by statistical moiré analysis and measured by energy dispersive X-ray spectroscopy. First, the addition of nitrogen in In(Ga)As QDs gave rise to a strong redshift in the emission peak, together with a large loss of intensity and monochromaticity. Moreover, these samples showed changes in the QDs morphology as well as an increase in the density of defects. The statistical compositional analysis displayed a normal distribution in InAs QDs with an average In content of 0.7. Nevertheless, the addition of Ga and/or N leads to a bimodal distribution of the Indium content with two separated QD populations. We suggest that the nitrogen incorporation enhances the indium fixation inside the QDs where the indium/gallium ratio plays an important role in this process. The strong redshift observed in the PL should be explained not only by the N incorporation but also by the higher In content inside the QDs

TMS- EEG Signatures of GABAergic Neurotransmission in the Human Cortex

Combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG) constitutes a powerful tool to directly assess human cortical excitability and connectivity. TMS of the primary motor cortex elicits a sequence of TMS-evoked EEG potentials (TEPs). It is thought that inhibitory neurotransmission through GABA-A receptors (GABAAR) modulates early TEPs (<50 ms after TMS), whereas GABA-B receptors (GABABR) play a role for later TEPs (at ∼100 ms after TMS). However, the physiological underpinnings of TEPs have not been clearly elucidated yet. Here, we studied the role of GABAA/B-ergic neurotransmission for TEPs in healthy subjects using a pharmaco-TMS-EEG approach. In Experiment 1, we tested the effects of a single oral dose of alprazolam (a classical benzodiazepine acting as allosteric-positive modulator at α1, α2, α3, and α5 subunit-containing GABAARs) and zolpidem (a positive modulator mainly at the α1 GABAAR) in a double-blind, placebo-controlled, crossover study. In Experiment 2, we tested the influence of baclofen (a GABABR agonist) and diazepam (a classical benzodiazepine) versus placebo on TEPs. Alprazolam and diazepam increased the amplitude of the negative potential at 45 ms after stimulation (N45) and decreased the negative component at 100 ms (N100), whereas zolpidem increased the N45 only. In contrast, baclofen specifically increased the N100 amplitude. These results provide strong evidence that the N45 represents activity of α1-subunit-containing GABAARs, whereas the N100 represents activity of GABABRs. Findings open a novel window of opportunity to study alteration of GABAA-/GABAB-related inhibition in disorders, such as epilepsy or schizophrenia.