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    Pharmacological discrimination between muscarinic receptor signal transduction cascades with bethanechol chloride

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    Authors
    Liu, Liwang
    Rittenhouse, Ann R.
    UMass Chan Affiliations
    Department of Physiology
    Program in Neuroscience
    Document Type
    Journal Article
    Publication Date
    2003-04-25
    Keywords
    Animals
    Animals, Newborn
    Bethanechol
    Calcium Channels, L-Type
    Calcium Channels, N-Type
    Calcium Signaling
    Egtazic Acid
    Muscarinic Agonists
    Oxotremorine
    Patch-Clamp Techniques
    Pertussis Toxin
    Rats
    Rats, Sprague-Dawley
    Receptor, Muscarinic M2
    Receptor, Muscarinic M4
    Signal Transduction
    Superior Cervical Ganglion
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573771/
    Abstract
    1. Muscarinic agonist specificity is limited, making it difficult to match receptor subtypes with signal transduction cascades that mediate ion channel modulation. We have characterized the inhibitory effects of two muscarinic agonists, oxotremorine-M (Oxo-M) and bethanechol chloride (BeCh), on Ca(2+) currents in neonatal rat superior cervical ganglion neurons. 2. Oxo-M-mediated (10 micro M) inhibition occurred via two signaling pathways. The first pathway inhibited whole cell peak currents, consisting primarily of N-type current, but not FPL 64176-induced, long-lasting tail currents, comprised entirely of L-type current. Inhibited currents displayed slowed activation kinetics and voltage dependence, characteristics of membrane-delimited inhibition. Current inhibition was blocked by the selective M(2) receptor antagonist, methoctramine (METH; 100 nM), or following pertussis toxin (PTX) pretreatment. 3. Activation of the second pathway inhibited both peak and long-lasting tail currents. This pathway was voltage-independent, PTX-insensitive, but sensitive to internal Ca(2+) chelator concentration. Muscarinic toxin 7 (MT-7, 100 nM), an irreversible M(1) receptor antagonist, eliminated this inhibition. Oxo-M (100 micro M) decreased L- and N-type channel activities in cell-attached patches, indicating that a diffusible second messenger is involved. 4. BeCh (100 micro M) also inhibited whole cell currents via the membrane-delimited pathway. Blocking M(4) receptors with 100 nM pirenzepine (in the presence of MT-7) had no effect, while antagonizing M(2) receptors with METH abolished inhibition. Concentrations of BeCh as high as 3 mM failed to inhibit either peak or long-lasting tail currents following PTX pretreatment. 5. These results indicate that BeCh may be an effective tool for selectively activating M(2) receptor stimulation of the membrane-delimited pathway.
    Source

    Br J Pharmacol. 2003 Apr;138(7):1259-70. Link to article on publisher's site

    DOI
    10.1038/sj.bjp.0705157
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/40455
    PubMed ID
    12711626
    Related Resources

    Link to article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.bjp.0705157
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