ArticleBritish journal of pharmacology2005
The antidepressant imipramine inhibits M current by activating a phosphatidylinositol 4,5-bisphosphate (PIP2)-dependent pathway in rat sympathetic neurones.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Investigating the Impact of Selective Modulators on the Renin-Angiotensin-Aldosterone System: Unraveling Their Off-Target Perturbations of Transmembrane Ionic Currents.International journal of molecular sciences · 2023Review
- Evidence for Effective Multiple KFrontiers in pharmacology · 2019Article
- The Cooperative Relationship between STAT5 and Reactive Oxygen Species in Leukemia: Mechanism and Therapeutic Potential.Cancers · 2018Review
- G protein-linked signaling pathways in bipolar and major depressive disorders.Frontiers in genetics · 2013Article
- Ca2+ signal summation and NFATc1 nuclear translocation in sympathetic ganglion neurons during repetitive action potentials.Cell calcium · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about the intracellular actions of imipramine (IMI) in the regulation of ion channels. We tested the action of IMI on the intracellular cascade that regulates M current (I(M)) in superior cervical ganglion neurones (SCGs). Dialysis of the cells with GDPbetaS, a G protein signaling blocker, did not disrupt the inhibition of I(M). When we incubated the cells with the phospholipase C (PLC) inhibitor U73122, it prevented the I(M) inhibition by IMI. Also, when we dialyzed the cells with an intracellular Ca2+ chelator, it did not disrupt I(M) inhibition by IMI, as occurs in the M1 cascade. When we incubated the cells with the generic kinase inhibitor wortmannin, it prevented the recovery of I(M) from the inhibition by IMI. Also, when we applied phosphatidylinositol 4,5-bisphosphate (PIP2) intracellularly, it diminished the inhibition of I(M) by IMI. Our findings suggest that PLC is the target for IMI, that recovery of I(M) needs lipid phosphorylation for PIP2 resynthesis, and that IMI inhibits I(M) by activating a PLC-dependent pathway, likely by decreasing the concentration of PIP2.
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