Site-controlled growth of quantum dots (QDs) for single photon emitters (SPEs) is achieved applying a buried stressor approach. Theoretical and experimental analysis shows that site-controlled QD growth on buried oxide stressor-layers benefits enormously from a defect-free growth interface. Laterally modulated strain fields at GaAs(001) growth surfaces are used to tailor surface morphologies at the centre of prescribed mesa structures for subsequent QD growth. Suitable morphologies for site-controlled QD growth such as nano-hillocks and nanoholes are identified. Site-controlled QD growth appears above the boundaries between the oxidised layer and the non-oxidised semiconductor layer. Through fine tuning of wetting layer thickness and growth interruption high selectivity for QD nucleation is achieved. Thus, growth of single QDs at the centre of a current-injection limiting aperture is demonstrated. Moreover, the QD growth on a defect-free surface yields high quality optical properties in terms of narrow emission linewidth and temporal stability with no discernible difference to QDs grown on planar substrates. The technological simplicity of the buried stressor approach and the inherent integration of a current aperture for efficient carrier injection into site-selected QDs enable mass production of SPEs on large substrate sizes.

Sharp wave–ripples (SWRs) are important for memory consolidation. Their signature in the hippocampal extracellular field potential can be decomposed into a ≈100 ms long sharp wave superimposed by ≈200 Hz ripple oscillations. How ripple oscillations are generated is currently not well understood. A promising model for the genesis of ripple oscillations is based on recurrent interneuronal networks (INT‐INT). According to this hypothesis, the INT‐INT network in CA1 receives a burst of excitation from CA3 that generates the sharp wave, and recurrent inhibition leads to an ultrafast synchronization of the CA1 network causing the ripple oscillations; fast‐spiking parvalbumin‐positive basket cells (PV+ BCs) may constitute the ripple‐generating interneuronal network. PV+ BCs are also coupled by gap junctions (GJs) but the function of GJs for ripple oscillations has not been quantified. Using simulations of CA1 hippocampal networks of PV+ BCs, we show that GJs promote synchrony beyond a level that could be obtained by only inhibition. GJs also increase the neuronal firing rate of the interneuronal ensemble, while they affect the ripple frequency only mildly. The promoting effect of GJs on ripple oscillations depends on fast GJ transmission (0.5 ms), which requires proximal GJ coupling (100 μm from soma), but is robust to variability in the delay and the amplitude of GJ coupling.

Sharp wave-ripple (SWRs) are important for memory consolidation. Their signature in the hippocampal extracellular field potential (EFP) can be decomposed into a ≈ 100 ms long sharp wave superimposed by ≈ 200 Hz ripple oscillations. How ripple oscillations are generated is currently not well understood. A promising model for the genesis of ripple oscillations is based on recurrent interneuronal networks (INT-INT). According to this hypothesis, the INT-INT network in CA1 receives a burst of excitation from CA3 that generates the sharp wave, and recurrent inhibition leads to an ultrafast synchronization of the CA1 network causing the ripple oscillations; fast-spiking parvalbumin-positive basket cells (PV+BCs) may constitute the ripple-generating interneuronal network.PV+BCs are also coupled by gap junctions (GJs) but the function of GJs for ripple oscillations has not been quantified. Using simulations of CA1 hippocampal networks of PV+BCs, we show that GJs promote synchrony and increase the neuronal firing rate of the interneuronal ensemble, while the ripple frequency is only affected mildly. The promoting effect of GJs on ripple oscillations depends on fast GJ transmission ( 0.5 ms), which requires proximal gap junction coupling ( 100 µm from soma).We thank Natalie Schieferstein for valuable comments on the manuscript.

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