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Neurochem Res ; 33(8): 1574-81, 2008 Aug.
Article in English | MEDLINE | ID: mdl-18404376

ABSTRACT

The Na(+)/H(+) exchanger has been the only unequivocally demonstrated H(+)-transport mechanism in the synaptosomal preparation. We had previously suggested that a Cl(-)-H(+) symporter (in its acidifying mode) is involved in cytosolic pH regulation in the synaptosomal preparation. Supporting this suggestion, we now show that: (1) when synaptosomes are transferred from PSS to either gluconate or sulfate solutions, the Fura-2 ratio remains stable instead of increasing as it does in 50 mM K solution. This indicates that these anions do not promote a plasma membrane depolarization. (2) Based in the recovery rate from the cytosolic alkalinization, the anionic selectivity of the Cl(-)-H(+) symporter is NO(3)(-) > Br(-) > Cl(-) >> I(-) = isethionate = sulfate = methanesulfonate = gluconate. (3) PCMB 10 muM inhibits the gluconate-dependent alkalinization by 30 +/- 6%. (4) Neither Niflumic acid, 9AC, Bumetanide nor CCCP inhibits the recovery from the cytosolic alkalinization.


Subject(s)
Anions/metabolism , Antiporters/genetics , Antiporters/metabolism , Brain/metabolism , Synaptosomes/metabolism , Amino Acid Sequence , Animals , Arylsulfonates/metabolism , Bumetanide/metabolism , Calcium/metabolism , Carbonyl Cyanide m-Chlorophenyl Hydrazone/metabolism , Fluorescent Dyes/metabolism , Gluconates/metabolism , Hydrogen-Ion Concentration , Ionophores/metabolism , Niflumic Acid/metabolism , Potassium/metabolism , Rats , Sodium Potassium Chloride Symporter Inhibitors/metabolism , Sulfates/metabolism
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