Effect of somatotrophic hormone in synaptosomal membrane Na,K-ATPase in the young rat brain

1988 ◽  
Vol 105 (5) ◽  
pp. 634-636
Author(s):  
V. V. Shkolovoi ◽  
G. N. Kryzhanovskii ◽  
R. N. Glebov
1996 ◽  
Vol 719 (1-2) ◽  
pp. 225-228 ◽  
Author(s):  
F. Fumagalli ◽  
S.R. Jones ◽  
M.G. Caron ◽  
F.J. Seidler ◽  
T.A. Slotkin

2006 ◽  
Vol 1078 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Márcio R. Martins ◽  
Adalisa Reinke ◽  
Fabrícia C. Petronilho ◽  
Karin M. Gomes ◽  
Felipe Dal-Pizzol ◽  
...  
Keyword(s):  

1994 ◽  
Vol 267 (5) ◽  
pp. R1273-R1279 ◽  
Author(s):  
F. Thies ◽  
C. Pillon ◽  
P. Moliere ◽  
M. Lagarde ◽  
J. Lecerf

The uptake and metabolism of [3H]docosahexaenoic acid (DHA) esterified at the sn-2 position of lysophosphatidylcholine (lysoPC DHA) and in the unesterified form, both bound to albumin, was studied in 20-day-old rats. LysoPC DHA was preferentially recovered in the brain (4-5% of the injected radioactivity) over the unesterified form of DHA (0.3-0.4%). Conversely, the lysoPC form was taken up less than or at the same extent as the unesterified form by the liver, heart, and kidney. In the brain, DHA was mainly recovered in phosphatidylethanolamine whether the esterified or the unesterified form was used, although DHA from lysoPC was esterified at the same extent in phosphatidylcholine and phosphatidylethanolamine after 2.5 min. The uptake of labeled palmitic, oleic, linoleic, and arachidonic acids, esterified or not in lysophosphatidylcholine, was also studied in brain, liver, heart, and kidney. Only the brain preferentially incorporated unsaturated (but not saturated) lysoPC, with the uptake increasing with the degree of unsaturation of the fatty acid moiety. These results strongly suggest that the young rat brain specifically utilizes albumin-lysoPC-containing polyunsaturated fatty acids.


1987 ◽  
Vol 63 (7) ◽  
pp. 846-852
Author(s):  
Masatomo MORI ◽  
Masako AKUZAWA ◽  
Toshio MICHIMATA ◽  
Masafumi YAMAGUCHI ◽  
Tokuji IRIUCHIJIMA ◽  
...  
Keyword(s):  

1999 ◽  
Vol 34 (6) ◽  
pp. 509-516 ◽  
Author(s):  
Teresa Iantomasi ◽  
Fabio Favilli ◽  
Maria T Vincenzini

1988 ◽  
Vol 91 (2) ◽  
pp. 289-303 ◽  
Author(s):  
D A Nachshen ◽  
P Drapeau

Cytosolic pH (pHi) was measured in presynaptic nerve terminals isolated from rat brain (synaptosomes) using a fluorescent pH indicator, 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The synaptosomes were loaded with BCECF by incubation with the membrane-permanent acetoxy-methyl ester derivative of BCECF, which is hydrolyzed by intracellular esterases to the parent compound. pHi was estimated by calibrating the fluorescence signal after permeabilizing the synaptosomal membrane by two different methods. Synaptosomes loaded with 15-90 microM BCECF were estimated to have a pHi of 6.94 +/- 0.02 (mean +/- standard error; n = 54) if the fluorescence signal was calibrated after permeabilizing with digitonin; a similar value was obtained using synaptosomes loaded with 10 times less BCECF (6.9 +/- 0.1; n = 5). When the fluorescence signal was calibrated by permeabilizing the synaptosomal membrane to H+ with gramicidin and nigericin, pHi was estimated to be 7.19 +/- 0.03 (n = 12). With the latter method, pHi = 6.95 +/- 0.09 (n = 14) when the synaptosomes were loaded with 10 times less BCECF. Thus, pHi in synaptosomes was approximately 7.0 and could be more precisely monitored using the digitonin calibration method at higher BCECF concentrations. When synaptosomes were incubated in medium containing 20 mM NH4Cl and then diluted into NH4Cl-free medium, pHi immediately acidified to a level of approximately 6.6. After the acidification, pHi recovered over a period of a few minutes. The buffering capacity of the synaptosomes was estimated to be approximately 50 mM/pH unit. Recovery was substantially slowed by incubation in an Na-free medium, by the addition of amiloride (KI = 3 microM), and by abolition of the Nao/Nai gradient. pHi and its recovery after acidification were not affected by incubation in an HCO3-containing medium; disulfonic stilbene anion transport inhibitors (SITS and DIDS, 1 mM) and replacement of Cl with methylsulfonate did not affect the rate of recovery of pHi. It appears that an Na+/H+ antiporter is the primary regulator of pHi in mammalian brain nerve terminals.


1989 ◽  
Vol 94 (2) ◽  
pp. 119-122
Author(s):  
Wasako ODA-KURIO ◽  
Reiko FUKUNAGA ◽  
Chiyoko INAGAKI

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