Abstract
The ionic conductances underlying the action potential and after-hyperpolarization of the cat petrosal ganglion neurones with myelinated axons in the carotid nerve were studied in vitro. Neurones were divided into two groups based on the presence or absence of an inflexion or hump on the spike falling phase. The application of tetrodotoxin (TTX, 3 X 10(-7)-3 X 10(-6) M) revealed the presence of a TTX-resistant component in spikes with a hump, which was abolished in Na+-free solution. The action potential without a hump was blocked by TTX. The spike hump decreased or was abolished when Ca2+-channel blockers (Mn2+, 3-4 mM or Co2+, 5 mM) or low-Ca2+ solutions (0.1-0.2 mM) were applied to the preparation. In neurones with a hump on the spike, regenerative responses were obtained in Na+-free, high-Ca2+ (8.8 mM) solution; these responses were antagonized by Mn2+, and their amplitude was proportional to the external Ca2+ concentration. It is concluded that the action potential with a hump was produced by an Na+ current, a part of which was TTX-resistant, and by a Ca2+ current which is responsible for the hump. Neurones without a hump had a TTX-sensitive Na+ spike. The spike with a hump was followed by a long-lasting after-hyperpolarization which reversed polarity at about -82 mV. During the hyperpolarization an increase in membrane conductance was observed. The amplitude and duration of the long hyperpolarizing potential decreased when Ca2+-channel blockers or low-Ca2+ solutions were applied. In Na+-free solution, regenerative responses were followed by a long hyperpolarization associated with an increase in membrane conductance. It is concluded that the long after-hyperpolarization is produced by activation of the Ca2+-dependent K+ conductance.
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