Carbachol induces inward current in rat neostriatal neurons through a G-protein-coupled mechanism

Kuei-Sen Hsu, Cheng Hsun Yang, Chiung Chun Huang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Our recent study demonstrated that carbachol can act at M1-like muscarinic receptors to reduce the membrane K+ conductance and excite the neostriatal neurons. In the present study, we further studied the molecular mechanism by which carbachol induced inward currents in neostriatal neurons. In acutely isolated neostriatal neurons held at -60 mV, pressure application of carbachol (30 μM) induced a transient inward current underlying whole-cell voltage-clamp mode. In cells loaded with the stable GDP analogue guanosine 5'-0-(2-thiodiphosphate) (GDP-β-S, 1 mM), the carbachol-induced inward current was significantly diminished. However, the carbachol response was not affected by intracellular dialysis of the neostriatal neurons with either protein kinase C (PKC) inhibitors, PKCI 19-36 (5 μM) or NPC-15437 (20 μM), or a potent cAMP-dependent protein kinase (PKA) inhibitor, Rp-cAMPS (25 μM). These results show that a G-protein-coupled mechanism mediates carbachol-induced inward current in the neostriatal neurons and that neither PKC- nor PKA-dependent intracellular transduction pathways are involved in the carbachol response.

Original languageEnglish
Pages (from-to)79-82
Number of pages4
JournalNeuroscience Letters
Volume224
Issue number2
DOIs
Publication statusPublished - 1997 Mar 14

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Carbachol
GTP-Binding Proteins
Neurons
Protein Kinase Inhibitors
Protein Kinase C
Muscarinic M1 Receptors
Protein C Inhibitor
Guanosine
Cyclic AMP-Dependent Protein Kinases
Protein Kinases
Dialysis
Pressure
Membranes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

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abstract = "Our recent study demonstrated that carbachol can act at M1-like muscarinic receptors to reduce the membrane K+ conductance and excite the neostriatal neurons. In the present study, we further studied the molecular mechanism by which carbachol induced inward currents in neostriatal neurons. In acutely isolated neostriatal neurons held at -60 mV, pressure application of carbachol (30 μM) induced a transient inward current underlying whole-cell voltage-clamp mode. In cells loaded with the stable GDP analogue guanosine 5'-0-(2-thiodiphosphate) (GDP-β-S, 1 mM), the carbachol-induced inward current was significantly diminished. However, the carbachol response was not affected by intracellular dialysis of the neostriatal neurons with either protein kinase C (PKC) inhibitors, PKCI 19-36 (5 μM) or NPC-15437 (20 μM), or a potent cAMP-dependent protein kinase (PKA) inhibitor, Rp-cAMPS (25 μM). These results show that a G-protein-coupled mechanism mediates carbachol-induced inward current in the neostriatal neurons and that neither PKC- nor PKA-dependent intracellular transduction pathways are involved in the carbachol response.",
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Carbachol induces inward current in rat neostriatal neurons through a G-protein-coupled mechanism. / Hsu, Kuei-Sen; Yang, Cheng Hsun; Huang, Chiung Chun.

In: Neuroscience Letters, Vol. 224, No. 2, 14.03.1997, p. 79-82.

Research output: Contribution to journalArticle

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