Previous work has shown that corticosterone facilitates the recruitment of GluA2-AMPARs by enhancing lateral diffusion, and increases both GluA2-AMPAR synaptic surface content and surface mobility in cultured hippocampal neurons [10], [11].
We describe the receptor dynamics by a combination of lateral diffusion and MT-dependent transport.
Thus, fluorescence recovery occurs by lateral diffusion and not transport across the nuclear membrane, which occurs over longer times than the characteristic time of diffusional recovery.
We introduce a simple correction procedure for lateral diffusion and demonstrate how the effect of lateral diffusion on diffusion in the DBL can be accounted for.
AMPARs exit post-synaptic densities (PSDs) by lateral diffusion and are endocytosed into clathrin-coated pits at sites near PSDs.
Fits of these equations to the simulated and literature data sets were computed using (1) Aeff = 3.8 cm or Aeff = 3.08 cm, as appropriate, (2) correction for lateral diffusion inside the sampler only (kLD, explanation in Results and Discussion), and (3) correction for lateral diffusion and non-1D diffusion through the DBL (kLD and kDBL, explanation in Results and Discussion).
Thus, the linear sweep voltammetry studies and previous literature provide supporting evidence for the absence of lateral diffusion and nanometer-scale phase separation on the gold surfaces.
The conclusions of the present study and those of Warnken et al. on the effect of lateral diffusion and the DBL on DGT measurements differ considerably.
This domain acts as a lateral diffusion barrier and separates the endodermal plasma membrane into two distinct polar domains (Roppolo et al., 2011; Alassimone et al., 2010).
We infer that both membrane trafficking and lateral diffusion contribute to fluorescence recovery of GFP-KNOLLE in the plane of cell division, because energy-inhibitor-treated roots displayed significantly reduced but still substantial recovery.
