Proton electrochemical gradient: Driving and regulating neurotransmitter uptake

BioEssays ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 1600240 ◽  
Author(s):  
Zohreh Farsi ◽  
Reinhard Jahn ◽  
Andrew Woehler

Author(s):  
M.J Kuhar ◽  
U Scheffel ◽  
J Boja ◽  
I.F Carroll ◽  
E Shaya ◽  
...  


1977 ◽  
Vol 69 (5) ◽  
pp. 537-552 ◽  
Author(s):  
PM Cala

The nucleated high K, low Na red blood cells of the winter flounder demonstrated a volume regulatory response subsequent to osmotic swelling or shrinkage. During volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation after osmotic swelling is referred to as regulatory volume decrease (RVD) and was characterized by net K and water loss. Since the electrochemical gradient for K is directed out of the cell there is no need to invoke active processes to explain RVD. When osmotically shrunken, the flounder erythrocyte demonstrated a regulatory volume increase (RVI) back toward control cell volume. The water movements characteristic of RVI were a consequence of net cellular NaCl and KCl uptake with Na accounting for 75 percent of the increase in intracellular cation content. Since the Na electrochemical gradient is directed into the cell, net Na uptake was the result of Na flux via dissipative pathways. The addition of 10(-4)M ouabain to suspensions of flounder erythrocytes was without effect upon net water movements during volume regulation. The presence of ouabain did however lead to a decreased ration of intracellular K:Na. Analysis of net Na and K fluxes in the presence and absence of ouabain led to the conclusion that Na and K fluxes via both conservative and dissipative pathways are increased in response to osmotic swelling or shrinkage. In addition, the Na and K flux rate through both pump and leak pathways decreased in a parallel fashion as cell volume was regulated. Taken as a whole, the Na and K movements through the flounder erythrocyte membrane demonstrated a functional dependence during volume regulation.



1998 ◽  
Vol 788 (1-2) ◽  
pp. 215-222 ◽  
Author(s):  
Alesia M Wright ◽  
Jeffrey Bempong ◽  
Michael L Kirby ◽  
Rebecca L Barlow ◽  
Jeffrey R Bloomquist


1974 ◽  
Vol 61 (1) ◽  
pp. 27-34
Author(s):  
PETER GREENAWAY

The premoult stage in Austropotamobius pallipes is characterized by a net loss of calcium which increases from D0 to a maximum of 0.83 µmoles/g/h at D4. The concentration of ionized calcium in the haemolymph does not increase during the premoult stage although there is an increase in complexed calcium. The electrochemical gradient across the body surface is similar to that at the intermoult stage and favours calcium outflux. Possible routes for calcium net loss have been discussed and a mechanism for elimination of calcium has been proposed.



1988 ◽  
Vol 254 (3) ◽  
pp. R491-R498 ◽  
Author(s):  
S. F. Perry ◽  
G. Flik

Experiments were performed to determine whether gill transepithelial calcium fluxes in the freshwater trout (Salmo gairdneri) are passive or require active transport and to characterize the mechanisms involved. A comparison of the in vivo unidirectional flux ratios with the flux ratios calculated according to the transepithelial electrochemical gradients revealed that calcium uptake from the water requires active transport of Ca2+. The inhibition of calcium uptake by external lanthanum, the specific deposition of lanthanum on the apical surface of chloride cells, and the favorable electrochemical gradient for calcium across the apical membrane suggest that the initial step in branchial calcium uptake is the passive entry of calcium into the cytosol of chloride cells through apical channels that are permeable to calcium. The study of gill basolateral plasma membrane vesicles demonstrated the existence of a high-affinity calmodulin-dependent calcium-transporting system [half-maximal Ca2+ concentration (K0.5) = 160 nM, Vmax = 1.86 nmol.min-1.mg protein-1]. This system actively transports calcium from the cytosol of chloride cells into the plasma against a sizeable electrochemical gradient, thereby completing the transepithelial uptake of calcium. Calcium efflux occurs passively through paracellular pathways between chloride cells and adjacent pavement cells or between neighboring pavement cells.



2006 ◽  
Vol 62 (1) ◽  
pp. 238-251 ◽  
Author(s):  
Patrick G. Bray ◽  
Mathirut Mungthin ◽  
Ian M. Hastings ◽  
Giancarlo A. Biagini ◽  
Dauda K. Saidu ◽  
...  


2001 ◽  
Vol 12 (10) ◽  
pp. 2003-2011
Author(s):  
VOLKER VALLON ◽  
FLORIAN GRAHAMMER ◽  
KERSTIN RICHTER ◽  
MARKUS BLEICH ◽  
FLORIAN LANG ◽  
...  

Abstract. The electrochemical gradient for K+ across the luminal membrane of the proximal tubule favors K+ fluxes to the lumen. Here it was demonstrated by immunohistochemistry that KCNE1 and KCNQ1, which form together the slowly activated component of the delayed rectifying K+ current in the heart, also colocalize in the luminal membrane of proximal tubule in mouse kidney. Micropuncture experiments revealed a reduced K+ concentration in late proximal and early distal tubular fluid as well as a reduced K+ delivery to these sites in KCNE1 knockout (-/-), compared with wild-type (+/+) mice. These observations would be consistent with KCNE1-dependent K+ fluxes to the lumen in proximal tubule. Electrophysiological studies in isolated perfused proximal tubules indicated that this K+ flux is essential to counteract membrane depolarization due to electrogenic Na+-coupled transport of glucose or amino acids. Clearance studies revealed an enhanced fractional urinary excretion of fluid, Na+, Cl-, and glucose in KCNE1 -/- compared with KCNE1 +/+ mice that may relate to an attenuated transport in proximal tubule and contribute to volume depletion in these mice, as indicated by higher hematocrit values.



2021 ◽  
Vol 2 ◽  
Author(s):  
Christopher J. Law

Abstract Proton electrochemical gradient-driven multidrug efflux activity of representatives of the major facilitator superfamily (MFS) of secondary active transporters contributes to antimicrobial resistance of pathogenic bacteria. Integral to the mechanism of these transporters is a proposed competition between substrate and protons for the binding site of the protein. The current work investigated the competition between protons and antimicrobial substrate for binding to the Escherichia coli MFS multidrug/H+ antiporter MdtM by measuring the quench of intrinsic protein fluorescence upon titration of substrate tetraphenylphosphonium into a solution of purified MdtM over a range of pH values between pH 8.8 and 5.9. The results, which revealed that protons inhibit binding of substrate to MdtM in a competitive manner, are consistent with those reported in a study on the related MFS multidrug/H+ antiporter MdfA and provide further evidence that competition for binding between substrate and protons is a general feature of secondary multidrug efflux.



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