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Syntaxin 8 has been shown to form the SNARE complex with syntaxin 7, vti1b and endobrevin. These have been shown to function as the machinery for the homotypic fusion of late endosomes. Recently, we showed that syntaxins 7 and 8 cycle through the plasma membrane, and that the di-leucine-based motifs in the cytoplasmic domain of syntaxins 7 and 8 respectively function in their endocytic and exocytic processes. However, we could not elucidate the mechanism by which syntaxin 8 cycles through the plasma membrane. In this study, we constructed several different syntaxin 8 molecules by mutating putative di-leucine-based motifs, and analyzed their intracellular localization and trafficking. We found a di-leucine-based motif in the cytoplasmic domain of syntaxin 8. It is similar to that of syntaxin 7, and functions in its endocytosis. These results suggest that in the cytoplasmic domain, syntaxin 8 has two functionally distinct di-leucine-based motifs that act independently in its endocytic and exocytic processes. This is the first report on two di-leucine-based motifs in the same molecule acting independently in distinct transport pathways.
 A simple theoretical model considering cell membrane mechanosensitivity can accurately describe published experimental data on membrane area creeping and recovery, and on osmotic expansion and rupture. The model to data fit reveals real values of membrane tension and elasticity modulus, and the parameters describing membrane organization and kinetics of mechanosensitive membrane traffic, including small solute transport, water permeability, endocytosis, exocytosis, and caveolae formation. This estimation allows for separation and quantitative analysis of the participation of different processes constituting the response of plasmalemma to short time-scale membrane load. The predicted properties of the model were verified for membrane stretching at different osmotic pressures. Finally, a simple hypothesis concerning stressed cell membrane breakdown is postulated.
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
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