Cytoplasmic alkalinization induced by insulin through an activation of Na+H+ antiporter inhibits tyrosine hydroxylase activity in striatal synaptosomes

Salvatore Amoroso, Gianfranco Di Renzo, Maurizio Taglialatela, Lorella M T Canzoniero, Edward J. Cragoe, Lucio Annunziato

Research output: Contribution to journalArticle

Abstract

Insulin dose-dependently inhibited tyrosine hydroxylase (TH) activity and increased intrasynaptosomal pH (pHi) in rat striatal nerve endings. Both these effects of insulin on TH and pHi were prevented by the 5-(N-methyl-N-(guanidinocarbonylmethyl) amiloride (MGCMA), a putative selective inhibitor of the Na+H+ antiporter. Interestingly when, by changing the extracellular pH (pHo), the pHi was increased, from 7.1 up to 7.5, an equivalent inhibition of TH activity occurred. The inhibitory action exerted from insulin on TH activity disappeared when the hormone was added to synaptosomes whose pHi was lowered to 6.83. Collectively, the results of the present study showed that insulin inhibited TH activity in striatal synaptosomes. This effect seems to involve the activation of the Na+-H+ antiporter. This exchange system once activated, may induce an intrasynaptosomal alkalinization, a condition in which TH activity is inhibited.

Original languageEnglish
Pages (from-to)1279-1282
Number of pages4
JournalBiochemical Pharmacology
Volume41
Issue number9
DOIs
Publication statusPublished - May 1 1991

ASJC Scopus subject areas

  • Pharmacology

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