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The paired motorneurones in the metathoracic ganglion of the locust have non-spiking somata whereas the dorsal unpaired media (DUM) neurones have spiking somata. We have studied the electrical properties of two identified neurones in the metathoracic ganglion that have spiking axons innervating the same muscle: the fast extensor tibiae (FETi) motomeurone has a non-spiking soma and the dorsal unpaired median extensor tibiae (DUMETi) neurone has a spiking soma. The inward current of the peripheral axon spikes of both DUMETi and FETi is carried predominantly by Na+, since the spikes are blocked only by removal of Na+ or addition of tetrodotoxin (TTX). The inward current of the soma spike of DUMETi is carried by Na+ and Ca2+, since it is blocked by either removal of Na+, addition of TTX, or addition of Co2+. The non-spiking soma of FETi shows delayed rectification. When some of the outward K+ current is blocked by TEA or 3-AP, the soma is capable of generating overshooting action potentials. The inward current of the TEA-induced soma spike of FETi is carried by Na+ and Ca2+, since it is blocked by either removal of Na+, addition of TTX or addition of Co2+. Axotomy or treatment with colchicine converts the non-spiking soma of FETi into a spiking soma within 4 days. The inward current of the soma spike is carried predominantly by Na+, since it is blocked only by removal of Na+. Five days after axotomy of one of the peripheral axons of DUMETi, Na+ is sufficient for the generation of the soma spike. Increased excitability is also observed in the neuropil of DUMETi after axotomy. When some of the outward K+ current is blocked by Ba2+, the normal and axotomized somata of FETi and DUMETi are all capable of generating long duration Ba2+ action potentials that are blocked by addition of Co2+. The overshooting Ba2+ action potentials in all cases are similar in amplitude and duration. It is concluded that the soma membrane of DUMETi and FETi normally contains both Na+ and Ca2+ inward current channels. The normal difference in excitability between these two somata may result in part or entirely from differences in the outward K+ current. It is suggested that axotomy or colchicine treatment cause an increase in the number of active Na+ channels in the soma membrane, which overcomes any differences in the outward K+ current and results in both cells being able to produce soma spikes.
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Goodman et al. (1979) studied this question.
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