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International audience; Zinc, a suspected potentiator of learning and memory, is shown to affect exocytotic release and storage in neurotransmitter-containing vesicles. Structural and size analysis of the vesicular dense core and halo using transmission electron microscopy was combined with single-cell amperometry to study the vesicle size changes induced after zinc treatment and to compare these changes to theoretical predictions based on the concept of partial release as opposed to full quantal release. This powerful combined analytical approach establishes the existence of an unsuspected strong link between vesicle structure and exocytotic dynamics which can be used to explain the mechanism of regulation of synaptic plasticity by Zn 2+ through modulation of neurotransmitter release.

This isposter on our paper titled “Massive core/star formation triggered by cloud-cloud collision: effect of magnetic field”.Massive stars are important in astrophysics, however their formation process is not well understood. Cloud-cloud collision is a strong candidate for massive star formation. We study the effect of magnetic field on massive dense core formation in colliding unequal molecular clouds by performing magnetohydrodynamic simulations with sub-parsec resolution (0.015 pc) that can resolve the molecular cores. We show that a greater number of massive, gravitationally bound cores are formed in the strong magnetic field (4.0 µG) models than the weak magnetic field (0.1 µG) models. This is partly because the strong magnetic field suppresses the spatial shifts of the shocked layer that should be caused by the nonlinear thin shell instability. The spatial shifts promote the formation of low-mass dense cores in the weak magnetic field models. The strong magnetic fields also support low-mass dense cores against gravitational collapse. In the strong magnetic field (perpendicular andoblique to collision axis models), we found that massive bound cores are formed in filaments, which are roughly normal to magnetic field.

The deposition of amyloid plaques is considered one of the main microscopic features of Alzheimer's disease (AD). Since plaque formation can precede extensive neurodegeneration and it is the main clinical manifestation of AD, it constitutes a relevant target for new treatment and diagnostic approaches. Micro-Raman spectroscopy, a label-free technique, is an accurate method for amyloid plaque identification and characterization. Here, we present a high spatial resolution micro-Raman hyperspectral study in transgenic APPswePS1ΔE9 mouse brains, showing details of AD tissue biochemical and histological changes without staining. First we used stimulated micro-Raman scattering to identify the lipid-rich halo surrounding the amyloid plaque, and then proceeded with spontaneous (conventional) micro-Raman spectral mapping, which shows a cholesterol and sphingomyelin lipid-rich halo structure around dense-core amyloid plaques. The detailed images of this lipid halo relate morphologically well with dystrophic neurites surrounding plaques. Principal Component Analysis (PCA) of the micro-Raman hyperspectral data indicates the feasibility of the optical biomarkers of AD progression with the potential for discriminating transgenic groups of young adult mice (6-month-old) from older ones (12-month-old). Frequency-specific PCA suggests that plaque-related neurodegeneration is the predominant change captured by Raman spectroscopy, and the main differences are highlighted by vibrational modes associated with cholesterol located majorly in the lipid halo.

Recent experimental observations have shown evidence of an unexpected sudden drop-off in the dense core vesicles (DCVs) content at the ends of certain types of axon endings. This article seeks to determine whether these observations may be explained without modifying the parameters characterizing the ability of distal en passant boutons to capture and accumulate DCVs. We developed a mathematical model that is based on the conservation of captured and transiting DCVs in boutons. The model consists of 77 ordinary differential equations and is solved using a standard Matlab solver. We hypothesize that the drop in DCV content in distal boutons is due to an insufficient supply of anterogradely moving DCVs coming from the soma. As anterogradely moving DCVs are captured (and eventually destroyed) in more proximal boutons on their way to the end of the terminal, the fluxes of anterogradely moving DCVs between the boutons become increasingly smaller, and the most distal boutons are left without DCVs. We tested this hypothesis by modifying the flux of DCVs entering the terminal and found that the number of most distal boutons left unfilled increases if the DCV flux entering the terminal is decreased. The number of anterogradely moving DCVs in the axon can be increased either by the release of a portion of captured DCVs into the anterograde component or by an increase of the anterograde DCV flux into the terminal. This increase could lead to having enough anterogradely moving DCVs such that they could reach the most distal bouton and then turn around by changing molecular motors that propel them. The model suggests that this could result in an increased concentration of resident DCVs in distal boutons beginning with bouton 2 (the most distal is bouton 1). This is because in distal boutons, DCVs have a larger chance to be captured from the transiting state as they pass the boutons moving anterogradely and then again as they pass the same boutons moving retrogradely.

We report unexpectedly fast phase transitions inside the track as pressure and temperature develop after a swift heavy ion impact. By means of molecular dynamics simulations we reveal the origin of the core-shell fine structure observed in a-${\mathrm{Si}}_{}{\mathrm{O}}_{2}$ and a-${\mathrm{Si}}_{3}{\mathrm{N}}_{4}$, as well as the dense core in a-Si. The fine structure of the track is composed of two distinct amorphous phases that result from the different pressure levels in the core and in the shell during solidification. We link this behavior to the tetrahedral network present in these materials.

Lambl's excrescences (LEs) are unusual, yet significant etiology of thromboembolism. LEs are fibrous valvular strands typically occurring at coaptation lines of the left-sided valves. These occur from wear and tear of the valves and comprise of a dense core of collagenous and elastic fibrils enclosed by endothelium. Transesophageal echocardiography (TEE) remains the gold standard in its diagnosis. Asymptomatic LEs are closely monitored, while symptomatic lesions with history of thromboembolism are managed with antiplatelet drugs or are anticoagulated. Surgery is indicated in case of recurrent thromboembolic episodes occurring while on medications.