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  • Title: Post-stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea-pig uterine artery in vitro.
    Author: Morris JL, Gibbins IL, Jobling P.
    Journal: J Physiol; 2005 Jul 01; 566(Pt 1):189-203. PubMed ID: 15802294.
    Abstract:
    Vasodilatation produced by stimulation of preganglionic neurones in lumbar and sacral pathways to pelvic ganglia was studied using an in vitro preparation of guinea-pig uterine artery and associated nerves in a partitioned bath allowing selective drug application to the ganglia or artery. Arterial diameter was monitored using real time video imaging. Vasodilatations produced by hypogastric nerve stimulation (HN; 300 pulses, 10 Hz) were significantly larger and longer in duration than with pelvic nerve stimulation (N = 18). Stimulation of ipsilateral lumbar splanchnic nerves or ipsilateral third lumbar ventral roots also produced prolonged vasodilatations. Blockade of ganglionic nicotinic receptors (0.1-1 mM hexamethonium) delayed the onset and sometimes reduced the peak amplitude of dilatations, but slow dilatations persisted in 16 of 18 preparations. These dilatations were not reduced further by 3 microM capsaicin applied to the artery and ganglia, or ganglionic application of 1 microM hyoscine, 30-100 microM suramin or 10 microM CNQX. Dilatations were reduced slightly by ganglionic application of NK1 and NK3 receptor antagonists (SR140333, SR142801; 1 microM), but were reduced significantly by bathing the ganglia in 0.5 mM Ca2+ and 10 mM Mg2+. Intracellular recordings of paracervical ganglion neurones revealed fast excitatory postsynaptic potentials (EPSPs) in all neurones on HN stimulation (300 pulses, 10 Hz), and slow EPSPs (3-12 mV amplitude) in 25 of 37 neurones. Post-stimulus action potential discharge associated with slow EPSPs occurred in 16 of 37 neurones (firing rate 9.4 +/- 1.5 Hz). Hexamethonium (0.1-1 mM) abolished fast EPSPs. Hexamethonium and hyoscine (1 microM) did not reduce slow EPSPs and associated post-stimulus firing in identified vasodilator neurones (with VIP immunoreactivity) or non-vasodilator paracervical neurones. These results demonstrate a predominantly sympathetic origin of autonomic pathways producing pelvic vasodilatation in females. Non-cholinergic mediators of slow transmission in pelvic ganglia produce prolonged firing of postganglionic neurones and long-lasting dilatations of the uterine artery. This mechanism would facilitate maintenance of pelvic vasodilatation on stimulation of preganglionic neurones during sexual activity.
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