Literature DB >> 15262335

Differential expression of calcium channels in sympathetic and parasympathetic preganglionic inputs to neurons in paracervical ganglia of guinea-pigs.

P Jobling1, I L Gibbins, R J Lewis, J L Morris.   

Abstract

Neurons in pelvic ganglia receive nicotinic excitatory post-synaptic potentials (EPSPs) from sacral preganglionic neurons via the pelvic nerve, lumbar preganglionic neurons via the hypogastric nerve or both. We tested the effect of a range of calcium channel antagonists on EPSPs evoked in paracervical ganglia of female guinea-pigs after pelvic or hypogastric nerve stimulation. omega-Conotoxin GVIA (CTX GVIA, 100 nM) or the novel N-type calcium channel antagonist, CTX CVID (100 nM) reduced the amplitude of EPSPs evoked after pelvic nerve stimulation by 50-75% but had no effect on EPSPs evoked by hypogastric nerve stimulation. Combined addition of CTX GVIA and CTX CVID was no more effective than either antagonist alone. EPSPs evoked by stimulating either nerve trunk were not inhibited by the P/Q calcium channel antagonist, omega-agatoxin IVA (100 nM), nor the L-type calcium channel antagonist, nifedipine (30 microM). SNX 482 (300 nM), an antagonist at some R-type calcium channels, inhibited EPSPs after hypogastric nerve stimulation by 20% but had little effect on EPSPs after pelvic nerve stimulation. Amiloride (100 microM) inhibited EPSPs after stimulation of either trunk by 40%, while nickel (100 microM) was ineffective. CTX GVIA or CTX CVID (100 nM) also slowed the rate of action potential repolarization and reduced afterhyperpolarization amplitude in paracervical neurons. Thus, release of transmitter from the terminals of sacral preganglionic neurons is largely dependent on calcium influx through N-type calcium channels, although an unknown calcium channel which is resistant to selective antagonists also contributes to release. Release of transmitter from lumbar preganglionic neurons does not require calcium entry through either conventional N-type calcium channels or the variant CTX CVID-sensitive N-type calcium channel and seems to be mediated largely by a novel calcium channel.

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Year:  2004        PMID: 15262335     DOI: 10.1016/j.neuroscience.2004.05.005

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  4 in total

1.  Alpha-ketoisocaproic acid increases phosphorylation of intermediate filament proteins from rat cerebral cortex by mechanisms involving Ca2+ and cAMP.

Authors:  Cláudia Funchal; Ariane Zamoner; André Quincozes dos Santos; Samanta Oliveira Loureiro; Moacir Wajner; Regina Pessoa-Pureur
Journal:  Neurochem Res       Date:  2005-09       Impact factor: 3.996

2.  Post-stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea-pig uterine artery in vitro.

Authors:  Judy L Morris; Ian L Gibbins; Phillip Jobling
Journal:  J Physiol       Date:  2005-03-31       Impact factor: 5.182

3.  Spontaneous release of acetylcholine from autonomic nerves in the bladder.

Authors:  V P Zagorodnyuk; S Gregory; M Costa; S J H Brookes; M Tramontana; S Giuliani; C A Maggi
Journal:  Br J Pharmacol       Date:  2009-04-03       Impact factor: 8.739

4.  Association of N-type calcium channel autoimmunity in patients with autoimmune autonomic ganglionopathy.

Authors:  Kurt Kimpinski; Valeria Iodice; Steve Vernino; Paola Sandroni; Phillip A Low
Journal:  Auton Neurosci       Date:  2009-06-21       Impact factor: 3.145

  4 in total

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