Muscarinic receptors activate calcium channels and calcium dependent potassium channels in NlE-115 neuroblastoma cells.

@article{Hedlund1987MuscarinicRA,
  title={Muscarinic receptors activate calcium channels and calcium dependent potassium channels in NlE-115 neuroblastoma cells.},
  author={Britta Hedlund and Matthias Lorentz and Peter {\AA}rhem},
  journal={Pharmacology \& toxicology},
  year={1987},
  volume={60 2},
  pages={
          156-60
        }
}
Responses of NlE-115 neuroblastoma cells to application of carbachol were studied using intracellular recording techniques. Activation of muscarinic cholinergic receptors by carbachol resulted in a depolarization of the cells. The response was blocked by pirenzepine (1 microM) and by CoCl2 (5 mM), verapamil (10 microM) and gallopamil (10 microM), and prolonged by quinine (5 mM). It is suggested that muscarinic receptors increase the membrane calcium permeability, and that the influx of calcium… 
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Alaproclate inhibits potassium currents and thereby enhances muscarinic stimulation in N1E-115 neuroblastoma cells
Morphine activates calcium channels in cloned mouse neuroblastoma cell lines
GEA 857 blocks potassium channels in the membrane and, thereby, prolongs muscarinic cholinergic responses in N1E-115 neuroblastoma cells.
TLDR
It is concluded that GEA 857 reduces potassium conductances in the membrane in N1E-115 neuroblastoma cells and, thereby, prolongs muscarinic agonist-induced responses.
Alaproclate increases the excitability of hippocampal CA1 pyramidal cells and blocks the slow after-hyperpolarization.
TLDR
Effects of alaproclate, an antidepressive substance and 5-HT uptake blocker, was studied using intracellular and extracellular recording techniques and it is suggested that these effects are due to depression of potassium channels in the membrane.
Exposure to carbachol induces several changes in muscarinic cholinergic parameters in N1E-115 mouse neuroblastoma cells.
TLDR
Mouse N1E-115 neuroblastoma cells were used to study carbachol induced changes in muscarinic cholinergic parameters, and changes observed in the choline esterase activity followed the same pattern.
Serotonin modulated Ca++ dependent K+ channels in alloimmune effector cell lytic function.
TLDR
Results indicate that 5-HT sensitive Ca++ dependent K+ channels are likely to be involved in the delivery of lytic signal(s) by immune effector lymphocytes and suggests that neuroendocrine products may modulate the functional activity of in vivo derived lymphocytes.
Regulation of intrasynaptosomal free calcium concentrations: studies with the fluorescent indicator, fluo-3
Role of K+ ion channels in lymphokine-activated killer (LAK) cell lytic function.
TLDR
It is demonstrated that K+ ion channels are involved in the LAK cell cytolytic process and that compounds, including neuroendocrine products, which modulate K- ion channel function are capable of modulating the lytic activity of these effector cells.
Kinetic analysis of K+ ion channel function in lymphokine-activated killer (LAK) cells.
TLDR
The K+ channel blocker, 4-aminopyridine, the neuroendocrine monoamine, serotonin, its agonist, quipazine, and the Ca++ dependent K+Channel blocker, quinidine were found to non-competitively inhibit the lytic process in a dose-dependent manner.
The cardiovascular response to medullary cholinergic and corticoid stimulation is calcium channel dependent in rats.
TLDR
The results suggest that the enhancement of cardiovascular activities mediated by cholinergic mechanisms may be due to the activation of postsynaptic calcium channels of neurons in the rVLM.
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References

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TLDR
Using voltage-clamped frog sympathetic neurones, this work has identified a distinctive voltage-sensitive K+ -current, separate from the delayed rectifier current, as the prime target for muscarinic agonists, and termed this current the M-current, IM.
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3':5'-cGMP levels of neuroblastoma N1E-115 cells increase as much as 200-fold upon activation of muscarinic acetylcholine receptors, resulting in intracellular cGMP concentrations greater than 600…
Responses of neuroblastoma cells to iontophoretically applied acetylcholine
TLDR
Dissociated mouse neuroblastoma cells were studied in vitro by using intracellular microelectrodes for electrical stimulation and recording to show changes in membrane potential to iontophoretically applied acetylcholine.
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TLDR
Examination of ionic membrane currents in a voltage-clamped neuronal cell line derived from the mouse C1300 neuroblastoma disclosed four kinetically different components: sodium, potassium, calcium, and leakage current, suggesting that the molecular structures of the sodium and potassium channels in neuroblastomas are similar to those of the non-mammalian preparations.
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TLDR
It is suggested that IM acts as a braking control on spike discharges and that removal of this control during slow cholinergic and peptidergic transmission provides a unique synaptic tuning mechanism.
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TLDR
It is concluded that Ca2+ entry during the action potential activates a TEA‐resistant K+ conductance which gives rise to the prolonged a.h.p. duration which plays a role in the regulation of low‐frequency firing.
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TLDR
Action potentials resulted from iontophoretic application of acetylcholine to cloned mouse neuroblastoma cells maintained in culture, suggesting an analogy with normal axons and dendrites.
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TLDR
The results are consistent with the hypothesis that IK(Ca) depends both on ICa and on membrane potential, and the slow K+ current is suggested to be mediated by Ca2+ influx, but the voltage‐dependence of the underlying conductance differs significantly from the ICa voltage-dependence.
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TLDR
Enter of Ca2+ into cells may increase cyclic GMP concentration by activating guanylate cyclase through an indirect mechanism.
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TLDR
It is concluded that separate voltage‐dependent Na+, K+ and Ca2+ channels exist in the differentiated neuroblastoma membrane with kinetic and pharmacological properties similar to those observed in non‐mammalian preparations.
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