Motoneurones form part of the final common pathway in the control of the musculature. Two modes of neurotransmitter action on neurones are distinguishable: neurotransmitters can gate ion channels directly or induce alterations in ion channel behaviour indirectly by way of second-messenger systems (Hille, 1992). In the former case the action is characterized by rapid onset and brief duration (milliseconds) whereas in the latter case the effects occur over longer time spans (seconds to minutes). In recent years it has become apparent that alterations in specific ionic conductances by neurotransmitters acting via second-messenger systems can modify motoneuronal behaviour.

Two neurotransmitters that produce their action primarily through second-messenger systems are the three-amino-acid peptide thyrotropin-releasing hormone (TRH), and the indolamine serotonin (5-HT). TRH and 5-HT are of interest because the source of these transmitters to various motoneurone pools appears to be the caudal raphe nuclei in the medulla oblongata, including raphe pallidus and obscurus (Holstege & Kuypers, 1987). Along with substance P (SP) these transmitters can be found co-localized within the same raphe neurone (Johansson et al., 1981). Neurones of raphe pallidus and obscurus alter their activity dramatically in different behavioural states (Jacobs & Azmitia, 1992), highest levels of activity occurring during waking and lowest levels during rapid-eye-movement (REM) sleep. It is therefore possible that TRH-, 5-HT- and SP-related inputs to motoneurones may vary with each state. An understanding of how these neurotransmitters affect motoneurones may provide new insights into changes in motor output that occur during various states (e.g. muscle atonia and reduced muscle reflexes in REM sleep).