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

Authors:
  • JRJ Ribas
    J Ribas
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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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