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. 1991;440:167–187. doi: 10.1113/jphysiol.1991.sp018702

Properties and ionic basis of the action potentials in the periaqueductal grey neurones of the guinea-pig.

D Sánchez 1, J Ribas 1
PMCID: PMC1180146  PMID: 1804959

Abstract

1. Action potentials of neurones of the ventral part of the guinea-pig periaqueductal grey (PAG) were studied by intracellular recording in a mesencephalic slice preparation maintained in vitro. 2. Fast spikes spontaneously fired last 2.8 +/- 0.6 ms (mean +/- S.D.) and have an amplitude of 72.3 +/- 5.3 mV (n = 28). The neurones could be antidromically activated from the neighbouring white matter and these spikes show an initial segment component that triggers the soma-dendritic spike. These two components were dissociated by hyperpolarization. Action potentials are Na+ dependent and a Ca2+ conductance is responsible for the hump on the falling phase. Hyperpolarization makes the hump disappear and a faster rate of rise and fall are seen. Accommodation of the firing threshold is observed in response to depolarizing ramps, which is eliminated with hyperpolarization. 3. High-threshold Ca2+ spikes are evoked in either Na(+)-free solution or in the presence of tetrodotoxin (TTX). These presumed dendritic action potentials display a fast repolarization and a large after-hyperpolarization (AHP) that prevent repetitive firing. This AHP is mainly generated by Ca(2+)-dependent K+ conductances. 4. The repolarization of fast action potentials depends on the activation of K+ conductances as well as a Na+ inactivation process. A fast-activated tetraethyl-ammonium (TEA)-sensitive K+ conductance, that could be Ca2+ dependent, and a K+ conductance blocked by apamin seem to be involved in the repolarization. 5. Each fast action potential is followed by a pronounced AHP with two components, an initial fast and a slow decaying phase. Membrane hyperpolarization around -60 mV eliminated the first component and the AHP acquired a plateau-like shape. At -90 mV the AHP was nullified. The slow phase was Ca2+ dependent and an apamin-sensitive K+ conductance is involved in its generation. This conductance may be active during the early part of the AHP, but a fast-activated TEA-sensitive K+ conductance and other voltage-dependent K+ conductances might also be present. A Ca2+ conductance is hypothesized to account for the fast depolarizing change after the AHP peak. 6. A delayed return to the baseline is observed after hyperpolarizing pulses. It is generated by the activation of a transient voltage-dependent K+ conductance that is inactive at resting membrane potential (RMP, around -50 mV). This transient hyperpolarization is abolished by Ca2+ channel blockers and insensitive to high external concentrations of 4-aminopyridine, TEA and Cs+.(ABSTRACT TRUNCATED AT 400 WORDS)

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Selected References

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