Serotonin (5-HT) is one of the main transmitters in the nervous system. Serotonergic neurons in the raphe nuclei in the brainstem
innervate most parts of the central nervous system including motoneurons in the spinal cord and brainstem. This review will focus
on the modulatory role that 5-HT exerts on motoneurons and its physiological consequences. The somato-dendritic compartments of motoneurons
are densely innervated by serotonergic synaptic boutons and several receptors are expressed in the membrane of motoneurons
including 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A, 5-HT2B, 5-HT2C and 5-HT5A. The activation of serotonergic receptors induces a general increase
of the excitability of motoneurons through the modulation of several classes of ion channels. 5-HT depolarizes motoneurons towards
the threshold for action potentials by inhibiting leak conductances and promoting a hyperpolarization activated cationic current. At
the same time, 5-HT increases the firing frequency by inhibiting the small Ca2+ activated K+ conductance (SK) responsible for the medium
afterhyperpolarization (AHP) following action potentials. 5-HT also promotes persistent inward currents mediated by voltage sensitive
Ca2+ and Na+ conductances, producing a sustained depolarization and an amplification of synaptic inputs. Under pathological conditions,
such as after a spinal cord injury, the promotion of persistent inward currents by serotonin and/or the overexpression of autoactive
serotonergic receptors may contribute to motoneuronal excitability, muscle spasms and spasticity and hence, impairment of stereotyped
motor behaviors such as locomotion, ejaculation and micturition.
Keywords: Serotonin, motoneuron, ion channel, modulation, plateau potential, afterhyperpolarization, neuroplasticity, fatigue, motor control,
spinal cord, brainstem, spinal cord injury.
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