Increase in [Ca2+]i by CCh in adult rat sympathetic neurons are not dependent on intracellular Ca2+ pools.

@article{Foucart1995IncreaseI,
  title={Increase in [Ca2+]i by CCh in adult rat sympathetic neurons are not dependent on intracellular Ca2+ pools.},
  author={Sylvain Foucart and Simon J. Gibbons and James R. Brorson and R. J. Miller},
  journal={The American journal of physiology},
  year={1995},
  volume={268 4 Pt 1},
  pages={
          C829-37
        }
}
We have examined the effects of the muscarinic agonists, carbachol (CCh) and oxotremorine (Oxo), on the intracellular free Ca2+ concentration ([Ca2+]i) in acutely dissociated sympathetic neurons from adult rats using fura 2-based microfluorometry. The drugs increased [Ca2+]i by 86 +/- 7 and 38 +/- 10 nM for CCh and Oxo, respectively (both 10 microM). Basal [Ca2+]i was 52 +/- 3 nM. Depletion of the caffeine-sensitive Ca2+ store or blockade of the Ca(2+)-adenosinetriphosphatase with thapsigargin… 
Muscarinic and nicotinic ACh receptor activation differentially mobilize Ca2+ in rat intracardiac ganglion neurons.
TLDR
Different signaling pathways mediate the rise in [Ca2+]i and membrane currents evoked by ACh binding to nicotinic and muscarinic receptors in rat intracardiac neurons, which is concomitant with slow outward currents on mAChR activation and with rapid inward currents after nA ChR activation.
Two different signaling mechanisms involved in the excitation of rat sympathetic neurons by uridine nucleotides.
TLDR
UTP inhibits M-type K(+) channels via an inositol trisphosphate-dependent signaling cascade that is also used by bradykinin but not by muscarinic acetylcholine receptors, and the secretagogue action of UTP is largely independent of this signaling cascade but involves pertussis toxin-sensitive G proteins.
Presynaptic Inhibition via a Phospholipase C- and Phosphatidylinositol Bisphosphate-Dependent Regulation of Neuronal Ca2+ Channels
TLDR
Results show that the presynaptic inhibition was mediated by a closure of voltage-gated Ca2+ channels through depletion of membrane phosphatidylinositol bisphosphates via phospholipase C.
Noradrenaline release from rat sympathetic neurones triggered by activation of B2 bradykinin receptors
TLDR
The role of bradykinin receptors in the regulation of sympathetic transmitter release was investigated in primary cultures of neurones dissociated from superior cervical ganglia of neonatal rats and data reveal bradykinsin as a potent stimulant of action potential‐mediated and Ca2+‐dependent release from rat sympathetic neurones.
Calcium Signalling in Neurons Exemplified by Rat Sympathetic Ganglion Cells
TLDR
Calcium (Ca2+) is essential for neural function and the mechanisms for Ca2+ entry, release, sequestration and extrusion vary somewhat from one type of nerve cell to another, but follow certain principles in common.
Sympathoexcitation by Bradykinin Involves Ca2+-Independent Protein Kinase C
TLDR
Results demonstrate that bradykinin B2receptors are linked to phospholipase C to simultaneously activate two signaling pathways: one mediates an inositol trisphosphate- and Ca2+-dependent inhibition of M-currents, the other one leads to an excitation of sympathetic neurons independently of changes in M- currents through an activation of Ca2-insensitive protein kinase C.

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TLDR
Intacellular bis(2-aminophenoxy)ethane-N,N, N,N',N'-tetraacetate (BAPTA) (11-12 mM), a Ca2+ chelator, reduced Ca2(+)-current suppression from 82 to 15% and is explained by a requirement for a certain minimum [Ca2+]i for continued operation of the pathway coupling muscarinic receptors to M-type K+ channels.
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TLDR
These studies suggest that the changes in [Ca2+]i produced by activation of muscarinic receptors result in part from mobilization of intracellular Ca2+ and that influx through voltage‐sensitive Ca 2+ channels also provides a significant contribution to the net [Ca 2+] i change observed.
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TLDR
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TLDR
Muscarinic modulation of the N-type Ca2+ channels appears to be mediated by a pertussis toxin-sensitive guanine nucleotide-binding protein and independent of both cAMP-dependentprotein kinase and protein kinase C.
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TLDR
The results suggest that the α2-autoreceptor-mediated inhibition of noradrenaline release from chick sympathetic neurons operates through the modulation of Ca2+ channels via pertussistoxin-sensitive GTP-binding-proteins.
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