The rate of vestibular osmolar and fluid increase is determined here by the rate of solute mixing and equilibration, k = 1 s−1, between the external solution and the external membrane surface.
No significant solute flow other than glucose occurs via GLUT2 between the external solution and vestibule.
With the increase of ionic strength in salt solution, the ionic osmotic pressure between the external solution and hydrogel decreases, so the water absorbency decreases.
Net water flow between the external solution [1] and the vestibule [2] is assumed to be entirely dependent on the osmotic pressure generated by the osmolar concentration difference between the external solution and the vestibular compartment [2].
Glucose flow between the external solution and the vestibule, Jg moles cm−2 s−1, has a maximal rate, Vm, between two saturable glucose binding sites facing the external and vestibular solutions.
As the equations make no specific provision for water transport, any associated water transport comes from other external factors, i.e., the osmotic relations involving water flow between the external solution and unstirred layer adjacent to the inside surface of the membrane (Fig. 1).
KCl and CsCl were accumulated from very low concentrations (of the order of 0.1 mM) but at concentrations as low as 10 mM there was no significant difference between their concentration in the external solution and that in the pores.
The neurons were then washed twice with external solution and incubated for 30 min at 37°C.
There are internal and external solutions, and Ripsaw is the latter.
The extent of elevation of intracellular calcium levels induced by acute application of 10 nM QDs in standard external solutions, calcium-free external solutions, thapsigargin-preincubated external solutions, and thapsigargin-preincubated calcium-free external solutions is expressed in Figure 3J.
