The action of high K+ and aglycaemia on the electrical properties and synaptic transmission in rat intracardiac ganglion neurones in vitro.
We have investigated the action of two elements of acute ischaemia, high potassium and aglycaemia, on the electrophysiological properties and ganglionic transmission of adult rat intracardiac ganglion (ICG) neurones. We used a whole-mount ganglion preparation of the right atrial ganglion plexus and sharp microelectrode recording techniques. Increasing extracellular K(+) from its normal value of 4.7 mm to 10 mm decreased membrane potential and action potential after-hyperpolarization amplitude but otherwise had no effect on postganglionic membrane properties. It did, however, reduce the ability of synaptically evoked action potentials to follow high-frequency (100 Hz) repetitive stimulation. A further increase in K(+) changed both the passive and the active membrane properties of the postganglionic neurone: time constant, membrane resistance and action potential overshoot were all decreased in high K(+) (20 mm). The ICG neurones display a predominantly phasic discharge in response to prolonged depolarizing current pulses. High K(+) had no impact on this behaviour but reduced the time-dependent rectification response to hyperpolarizing currents. At 20 mm, K(+) practically blocked ganglionic transmission in most neurones at all frequencies tested. Aglycaemia, nominally glucose-free physiological saline solution (PSS), increased the time constant and membrane resistance of ICG neurones but otherwise had no action on their passive or active properties or ganglionic transmission. However, the combination of aglycaemia and 20 mm K(+) displayed an improvement in passive properties and ganglionic transmission when compared with 20 mm K(+) PSS. These data indicate that the presynaptic terminal is the primary target of high extracellular potassium and that aglycaemia may have protective actions against this challenge.
Dyavanapalli
Jhansi
J
College of Life Sciences, University of Dundee, UK.
Rimmer
Katrina
K
Harper
Alexander A
AA
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000502:physiology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D055724:Electrophysiological Phenomena / Q000502:physiology*; D005260:Female; D005724:Ganglia / Q000502:physiology*; D006321:Heart / Q000294:innervation*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000494:pharmacology*; D017729:Presynaptic Terminals / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
D001786:Blood Glucose; D011188:Potassium