Abstract
The effects of 5-hydroxytryptamine (5-HT) on spinal motoneurons were examined in pentobarbital-anaesthetized cats and in nonanaesthetized decerebrate cats by intracellular recording and extracellular iontophoresis of 5-HT. 5-HT first induced a depolarization and then a long-lasting hyperpolarization (up to 60 min) with unchanged input resistance. The slow hyper-polarization was prevented by the 5-HT antagonists ketanserin (5-HT2), methysergide, and spiperone (5-HT1,2) and mimicked by the agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (5-HT2). The post-spike afterhyperpolarization was enhanced after application of 5-HT. A depolarization was induced by the 5-HT agonists (±)-8-hydroxy-(2)-(di-n-propylamino)tetralin (5-HT1A) and 1-(2-methoxyphenyl)piperazine (5-HT1). Possible mechanisms for the 5-HT-induced hyperpolarization and its intracellular mediation are discussed. The present data suggest multiple effects of 5-HT on cat spinal motoneurons.Key words: afterhyperpolarization, depolarization, 5-hydroxytryptamine, hyperpolarization, iontophoresis, spinal motoneuron.

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