Effects of nerve stimulation on the spontaneous action potentials recorded in the proximal renal pelvis of the guinea-pig

1995 ◽  
Vol 23 (5) ◽  
pp. 343-350 ◽  
Author(s):  
R. J. Lang ◽  
Y. Zhang ◽  
B. Exintaris ◽  
F. Vogalis
Keyword(s):  
Guinea Pig ◽  
Nerve Stimulation ◽  
Renal Pelvis ◽  
Action Potentials ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Spontaneous action potentials in isolated guinea-pig cerebellar slices: effects of amino acids and conditions affecting sodium and water uptake

1973 ◽  
Vol 184 (1074) ◽  
pp. 83-90 ◽  
Keyword(s):  
Amino Acids ◽  
Guinea Pig ◽  
Action Potentials ◽  
Excitatory Amino Acids ◽  
Quantitative Assessment ◽  
Ammonium Ions ◽  
Quantitative Correlation ◽  
Spontaneous Action ◽  
Inhibitory Amino Acids ◽  
Spontaneous Action Potentials

The effects of incubation conditions on the frequency of spontaneous action potentials exhibited by guinea-pig cerebellar slices, and recorded with an extracellular microelectrode, have been investigated. Various incubation conditions that lead to tetrodotoxin-sensitive uptakes of water and of sodium ions by the incubated cerebellar slices lead to enhanced frequencies of the spontaneous action potentials, e. g. the presence of protoveratrine or of ouabain, the absence of glucose or the onset of anoxia. The frequency of the spikes is also enhanced by acetylcholine (in presence of neostigmine) or by the presence of excitatory amino acids, such as L-glutamate, D-glutamate or L-aspartate. It is suppressed by tetrodotoxin, or by the inhibitory amino acids, e. g. γ -aminobutyrate, glycine or taurine, or by ammonium ions or by pentobarbital. It is concluded that guinea-pig cerebellar slices, incubated under specified conditions, may provide a suitable means for quantitative correlation of neurochemical data with data obtained by electrophysiological techniques in tissue incubated under similar conditions and also for quantitative assessment of the effects of amino acids on cerebellar electrical activity.

Response of Ca(2+)-loaded, depolarized guinea pig myocytes to critically timed premature stimulations

1996 ◽  
Vol 270 (2) ◽  
pp. H447-H465
Author(s):  
C. Nordin
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Action Potentials ◽  
Low Dose ◽  
Tyrode Solution ◽  
Coupling Interval ◽  
Spontaneous Action ◽  
Experimental Response ◽  
Spontaneous Action Potentials

Single premature stimulations during trains of nondriven action potentials induced by depolarization normally cause a transient hyperpolarization of diastolic membrane potential before the subsequent spontaneous upstroke. However, rare, marked transient depolarizations have also been reported. This paper presents experimental data and computer simulations that characterize transient depolarization following premature stimulations and investigate the role of intracellular [Ca2+] in generating this unusual response. In isolated guinea pig myocytes, transient depolarizations (range 4-58 mV) consistently occurred following stimulations 100-160 ms after the upstroke of spontaneous action potentials during exposure to K(+)-free Tyrode solution, which raises intracellular [Ca2+]. In contrast, no transient depolarizations developed when stimulations were delivered during injection of constant inward current or brief exposure to very low dose of Ba2+ (250-500 microM). The experimental response to K(+)-free Tyrode solution was reproduced by a computer model of the transmembrane current and intracellular Ca2+ flux of an isolated guinea pig ventricular myocyte (24) following reduction of extracellular [K+] below 1 mM. Transient depolarization was generated primarily by Na/Ca exchange. Simulations using only those equations governing intracellular Ca2+ cycling revealed that bursts of Ca2+ into the myoplasm after Ca2+ loading caused a transient increase in trough myoplasmic [Ca2+] when the coupling interval following the upstroke of a myoplasmic [Ca2+] oscillation was nearly identical to those coupling intervals that caused pacing-induced transient depolarization of membrane potential after the upstroke of an action potential. These results suggest that transient depolarizations following nondriven action potentials arise from critically timed, stimulus-induced perturbation of intracellular [Ca2+] oscillations associated with Ca2+ overload. Simulations using a multicellular model suggest that critically timed premature stimulations can initiate trains of depolarized, nondriven action potentials in otherwise quiescent, Ca(2+)-overloaded heterogeneous syncytia by a similar mechanism.

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