Post-stimulus potentiation of transmission in pelvic ganglia enhances sympathetic dilatation of guinea-pig uterine artery in vitro.
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.
Morris
Judy L
JL
Department of Anatomy & Histology, Center for Neuroscience, Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia. judy.morris@flinders.edu.au
Gibbins
Ian L
IL
Jobling
Phillip
P
D000818:Animals; D001158:Arteries / Q000294:innervation* / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D005725:Ganglia, Autonomic / Q000502:physiology; D005727:Ganglia, Spinal / Q000502:physiology*; D006168:Guinea Pigs; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D010388:Pelvis / Q000294:innervation / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D014599:Uterus / Q000098:blood supply* / Q000294:innervation* / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*