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Dimeric tubulin-stimulated adenylyl cyclase activity is augmented after long-term amitriptyline treatment

Authors
Journal
Life Sciences
0024-3205
Publisher
Elsevier
Publication Date
Volume
60
Issue
1
Identifiers
DOI: 10.1016/s0024-3205(96)00589-9
Keywords
  • Antidepressants
  • Tubulin
  • Gtp-Binding Protein
  • Signal Transduction
  • Adenylyl Cyclase
Disciplines
  • Biology

Abstract

Abstract We have investigated altered association of tubulin dimers interacting with G proteins and modulating adenylyl cyclase (AC) as a result of long-term amitriptyline (AMT) treatment. Gpp(NH)p-stimulated, but not basal or manganese-stimulated, AC activity was significantly augmented in cortex membranes prepared from rats chronically treated with AMT. The enhancement of AC activity by Gpp(NH)p-liganded tubulin (tubulin-Gpp(NH)p) was significantly higher in chronically AMT-treated rats than in control rats. Moreover, in cortex membranes from controls, tubulin-Gpp(NH)p prepared from chronically AMT-treated rats was more effective to activate AC activity than tubulin-Gpp(NH)p from controls. Immunoblotting and photoaffinity guanine nucleotide binding procedures showed no significant differences in the amount and the function of G proteins between controls and AMT-treated groups. It is suggested that long-term AMT treatment causes alteration in the functional interaction between tubulin and G protein, and this modification may participate in enhanced coupling of Gs to the catalytic subunit of AC induced by the chronic antidepressant treatment.

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