Nicotine induces calcium spikes in single nerve terminal varicosities: a role for intracellular calcium stores
Section snippets
Experimental procedures
Vasa deferentia were removed from 8–12-week-old Balb/c mice (Harlan, UK), which had been humanly killed by cervical fracture. All efforts were made to minimise the number of animals used and their suffering; all experiments were in accordance with the European Communities Council Directives (86/609/EEC of 24 November 1986) and approved by the local ethics committee (Department of Pharmacology, University of Oxford, Oxford, UK). A midline incision was made to expose the abdominal viscera and the
Results
The effect of nicotine on neurogenic contractions evoked by a train of 10 stimuli at 10 Hz was investigated in mouse vas deferens from which the sympathetic ganglia had been removed. Nicotine (10 μM) increased the force of the neurogenic contraction by 135±25% (n=6; P<0.01; Fig. 1A,C). The potentiating effect peaked about 30 s after the application of nicotine, after which the force of contraction returned towards its resting level. The time taken to return to control levels was not measured as
Discussion
The contraction studies demonstrate that nicotine acts within this tissue to increase the force of neurogenic contraction, an action previously attributed mainly to increased noradrenaline release (McGrath, 1978). The increase in the amplitude of EJPs and the increase in the frequency of SEJPs suggest that nicotine also acts on prejunctional sympathetic terminals to increase the release of the co-transmitter ATP, which is the neurotransmitter generating EJPs in the mouse vas deferens (Stjärne
Acknowledgements
K.L.B. was supported by a Sydney Tapping Postgraduate Research Award, The University of Sydney, Australia. S.J.T. is supported by The Wellcome Trust.
References (33)
- et al.
Impulse conduction in sympathetic nerve terminals in the guinea-pig vas deferens and the role of the pelvic ganglia
Neuroscience
(1992) Calcium permeability of ligand-gated channels
Cell Calcium
(1998)- et al.
The mechanism of action of nicotine on vascular adrenergic neuroeffector transmission
Eur. J. Pharmacol.
(1977) - et al.
The anti-dementia drug nefiracetam facilitates hippocampal synaptic transmission by functionally targeting presynaptic nicotinic ACh receptors
Mol. Brain Res.
(2000) - et al.
Acetylcholine differentially affects intracellular calcium via nicotinic and muscarinic receptors on the same population of neurons
J. Biol. Chem.
(1995) - et al.
Blockade of smoking satisfaction using the peripheral nicotinic antagonist trimethaphan
Pharmacol. Biochem. Behav.
(1999) - et al.
Discrete events measure single quanta of adenosine 5′-triphosphate secreted from sympathetic nerves of guinea-pig and mouse vas deferens
Neuroscience
(1984) - et al.
Absorption and metabolism of nicotine from cigarettes
Br. Med. J.
(1975) - et al.
An electrophysiological analysis of the effect of Ca ions on neuromuscular transmission in the mouse vas deferens
Br. J. Pharmacol.
(1975) - Benowitz, N.L., Jacob, P., 1987. In: Martin, W.R. et al., (Eds.), Tobacco Smoking and Nicotine: A Neurobiological...
Electrical events associated with the action of nicotine at the adrenergic nerve terminal
Arch. Int. Pharmacodyn.
Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition
J. Physiol.
Electrical activity at the sympathetic neuroeffector junction in the guinea-pig vas deferens
J. Physiol.
Presynaptic nicotinic receptors stimulate increases in intraterminal calcium of chick sympathetic neurons in culture
J. Neurochem.
Increase in [Ca2+]i by CCh in adult rat sympathetic neurons are not dependent on intracellular Ca2+ pools
Am. J. Physiol.
Hippocampal synaptic transmission enhanced by low concentrations of nicotine
Nature
Cited by (61)
High-energy compounds mobilize intracellular Ca<sup>2+</sup> and activate calpain in cultured cells: Is calpain an energy-dependent protease?
2014, Brain Research BulletinCitation Excerpt :Similar results were also obtained with two other HECs, PCr and ACoA (−ΔG°′ = 10.3 and 7.7 kcal/mol, respectively) (Lehninger, 1975) (data not shown). Thus, Ca2+ influx elicited by the HECs entered the cytosol from both extracellular medium and intracellular stores (through calcium release-activated calcium channels), similar to the mechanisms of nicotine and glutamate, two commonly used Ca2+ agonists (Brain et al., 2001; Schapansky et al., 2009). We also found that PEP, PCr and ACoA mobilized Ca2+ in a dose-dependent manner (Fig. 1d).
Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity
2010, Pharmacology and TherapeuticsCitation Excerpt :Diverse neurochemical changes associated with dendritic synaptic plasticity have been shown to rely on RyR function, including: 1) activity-dependent postsynaptic translation (Jourdi et al., 2009) and secretion (Kolarow et al., 2007) of neurotrophins, 2) modulation of Gq-coupled receptor function by stress peptides and hormones (Riegel & Williams, 2008); 3) activity-dependent enhancement of glutamate responses and the associated increase of GluR1 within spines mediated by synaptopodin, an actin-binding protein that co-localizes with RyRs within the spine apparatus of hippocampal neurons (Vlachos et al., 2009); and 4) sequential activation of CaM kinases, CREB and transcription of genes encoding Ca2+-regulated proteins triggered by repetitive or prolonged depolarization of hippocampal neurons (Deisseroth et al., 1998). RyRs similarly function in peripheral neurons to regulate the release of (Cong et al., 2004; Ouyang et al., 2005; Huang et al., 2008) and response to (Brain et al., 2001; Locknar et al., 2004) neurotransmitters and neuropeptides, and their function underlies the exocytotic release of glutamate from astrocytes (reviewed in Reyes & Parpura, 2009). Changes in postsynaptic efficacy are also associated with morphological changes in dendritic spines.
Intracellular Ca<sup>2+</sup> dynamics of hippocampal interneurons following nicotinic acetylcholine receptor activation
2008, Neurochemistry International