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
Calcium (Ca2+) is essential for neural function. The most obvious requirement is to trigger the release of transmitter when the action potential arrives at the axon terminals. However, Ca2+ can also
Nicotine induces calcium spikes in single nerve terminal varicosities: a role for intracellular calcium stores
TLDR
A novel mechanism is proposed whereby nicotine's action at nAChRs triggers calcium-induced calcium release from a ryanodine-sensitive calcium store in nerve terminals, which primes neurotransmitter release mechanisms and enhances both spontaneous and action potential-evoked neurotransmitterRelease.
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.
Mechanism of acetylcholine-induced calcium signaling during neuronal differentiation of P19 embryonal carcinoma cells in vitro.
TLDR
The presence of functional nAChRs in embryonic cells suggests that these receptors are involved in triggering Ca(2+) waves during initial neuronal differentiation.

References

SHOWING 1-10 OF 32 REFERENCES
Intracellular Ca2+ buffers disrupt muscarinic suppression of Ca2+ current and M current in rat sympathetic neurons.
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.
Muscarinic Agonists Cause Calcium Influx and Calcium Mobilization in Forebrain Neurons In Vitro
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.
The role of caffeine-sensitive calcium stores in the regulation of the intracellular free calcium concentration in rat sympathetic neurons in vitro.
TLDR
It is concluded that mammalian sympathetic neurons possess intracellular Ca2+ stores with pharmacological characteristics that closely resemble those found in muscle but that these are relatively small and produce little amplification of [Ca2+]i transients resulting from Ca2+.
Measurement of intracellular Ca2+ in the bullfrog sympathetic ganglion cells using fura-2 fluorescence
The intracellular free Ca2+ concentration ([Ca2+]i) of the bullfrog sympathetic ganglion cell was measured with fura-2 fluorescence under various conditions, and compared with changes in membrane
Muscarinic suppression of the M-current is mediated by a rise in internal Ca2+ concentration
TLDR
The hypothesis that the muscarinic suppression of M-current is mediated by the release of Ca2+ from intracellular stores is supported by the results of these experiments.
Imaging of cytosolic Ca2+ transients arising from Ca2+ stores and Ca2+ channels in sympathetic neurons
TLDR
Ca2+ release or uptake from caffeine-sensitive internal stores was able to amplify or attenuate the effects of Ca2+ influx, to generate continued oscillations in [Ca2-]i, and to persistently elevate [Ca 2+]i above basal levels after the stores had been Ca2(+)-loaded.
Modulation of M-current by intracellular Ca2+
TLDR
The results suggest that IM can be regulated by physiologically relevant changes in [Ca2+]i, placing IM in a unique position to modulate cell excitability.
Activation of a muscarinic receptor selectively inhibits a rapidly inactivated Ca2+ current in rat sympathetic neurons.
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.
Inhibition of Ca2+ and K+ channels in sympathetic neurons by neuropeptides and other ganglionic transmitters
TLDR
It is found that peptidergic inhibition of Ca2+ channels involves G proteins, but does not require protein kinases, and leads to reductions in Ca2(+)-activated K+ current and catecholamine release.
Pertussis toxin abolishes the inhibition of Ca2+ currents and of noradrenaline release via α2-adrenoceptors in chick sympathetic neurons
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.
...
1
2
3
4
...