The values of various diffusive behaviors of sPH-AP-QDs analyzed in this study.

<p>Actin, actin cytoskeleton disrupted; Microtubule, microtubule disrupted; Gly-SP, Glycine-induced synaptic potentiation; NMDA-SD, NMDA-induced synaptic depression; D_synapse, diffusion coefficient at synapses; D_ex-synapse, diffusion coefficient at extrasynapses; All values are mean ± s.e. *p<0.01, paired <i>t</i>-test.</p

Single QD tracking of synaptic vesicles using sPH-AP-QDs.

<p>(<b>A</b>) Hippocampal neurons were co-transfected with sPH-AP and Bir-ER at DIV 12, and labeled with 1 nM streptavidin-conjugated-QD at DIV17. Blue color: the functional presynaptic terminals were identified by sPH fluorescence change (ΔF). Scale bar, 20 µm. (<b>B</b>) Example of sPH-AP-QDs (red) trafficking along the axon (green). Arrows: sPH-AP-QDs trafficking between synaptic and extrasynaptic compartments, arrowheads: sPH-AP-QDs at presynaptic terminals. asterisks: functional presynaptic terminals (blue). Scale Bar, 2.5 µm. (<b>C</b>) Instantaneous displacement change of the moving sPH-AP-QD marked by the arrow in (<b>B</b>) from its initial location (displacement = 0) along the axon during recording sequence. The <i>x</i> and <i>y</i> coordinates of QD trajectory at each time point in time-lapse images were obtained using MetaMorph track object function and the displacement from the origin to the QD trajectory at each time point was calculated and plotted. The graph parallel to <i>y</i> axis means no movement. The upper lines denote the frames in which the sPH-AP-QD is at extrasynaptic areas (gray) and synapses (red and shaded areas). (<b>D</b>) MSD versus time, calculated for a continuous sequence of images, which show the synaptic motion (red) and extrasynaptic motion (blue). Inset represents average diffusion coefficient of sPH-AP-QDs at synapses (red) and at extrasynapses (blue).</p

Fluorescence Recovery after Merging a Surfactant-Covered Droplet: A Novel Technique to Measure the Diffusion of Phospholipid Monolayers at Fluid/Fluid Interfaces

We present a novel technique to measure diffusion coefficients of insoluble surfactant monolayers. We merge a surfactant-coated droplet with a fluorescently labeled planar monolayer. During the merging process, a monolayer on a droplet displaces the existing planar monolayer, leaving a dark area when viewed under a fluorescence microscope. We measure fractional intensities as the dyes recover, which allows diffusion coefficients to be computed. We validate this technique with the two most common phospholipid monolayers (DPPC and DOPC) and study the diffusion of their mixtures. The proposed technique has several advantages over the FRAP technique and is potentially capable of measuring the diffusion of any soluble/insoluble surfactant monolayers

Table_1_Shank2 Deletion in Parvalbumin Neurons Leads to Moderate Hyperactivity, Enhanced Self-Grooming and Suppressed Seizure Susceptibility in Mice.xlsx

<p>Shank2 is an abundant postsynaptic scaffolding protein implicated in neurodevelopmental and psychiatric disorders, including autism spectrum disorders (ASD). Deletion of Shank2 in mice has been shown to induce social deficits, repetitive behaviors, and hyperactivity, but the identity of the cell types that contribute to these phenotypes has remained unclear. Here, we report a conditional mouse line with a Shank2 deletion restricted to parvalbumin (PV)-positive neurons (Pv-Cre;Shank2^fl/fl mice). These mice display moderate hyperactivity in both novel and familiar environments and enhanced self-grooming in novel, but not familiar, environments. In contrast, they showed normal levels of social interaction, anxiety-like behavior, and learning and memory. Basal brain rhythms in Pv-Cre;Shank2^fl/fl mice, measured by electroencephalography, were normal, but susceptibility to pentylenetetrazole (PTZ)-induced seizures was decreased. These results suggest that Shank2 deletion in PV-positive neurons leads to hyperactivity, enhanced self-grooming and suppressed brain excitation.</p