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Intracellular studies showing modulation of facial motoneurone excitability by serotonin

Naturevolume 287pages346347 (1980) | Download Citation



The application of serotonin to certain myenteric plexus neurones in the guinea pig small intestine causes a slow depolarization of membrane potential, accompanied by increased neuronal excitability and input resistance1. On the other hand, microiontophoretic application of large amounts of serotonin onto mammalian spinal motoneurones is reported to cause membrane hyperpolarization and decreased excitability2. However, on the basis of recording spinal reflex activity, serotonin has been reported to enhance net motoneurone activity3. Moreover, studies using extracellular single-cell recording techniques indicate that serotonin in small amounts facilitates synaptically or glutamate-induced excitation of mammalian motoneurones in the facial nucleus4 and spinal cord5. It was suggested that these facilitatory actions were modulatory in nature, as serotonin did not induce motoneurone spiking in the absence of extrinsic excitatory input. The study reported here investigated the membrane mechanisms underlying these modulatory effects by obtaining intracellular recordings from rat facial motoneurones during extracellular microiontophoretic application of serotonin, methysergide (a serotonin antagonist) and noradrenaline. Serotonin caused a slow depolarization of membrane potential of about 5 mV which remained subthreshold, accompanied by an increase in electrical excitability of the neurone, and an increase in input resistance. Noradrenaline caused the same changes. Methysergide antagonized the effects of serotonin, but not noradrenaline, indicating that these actions of serotonin are selective and receptor mediated.

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  1. Departments of Psychiatry and Pharmacology, Yale University School of Medicine, 34 Park Street, New Haven, Connecticut, 06508

    • C. P. VanderMaelen
    •  & G. K. Aghajanian


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