The role of dopamine in directly modulating somatic motoneuron excitability and hence muscle tone is unknown. We investigated whether dopamine influences the trigeminal motor pool (MoV) that innervates the masseter and tensor palatini muscles, both of which function to maintain upper airway patency. We hypothesized that dopamine facilitates motor outflow at the MoV. We focally applied apomorphine (nonspecific dopamine receptor agonist) at the MoV in anaesthetized rats. We also applied receptor-specific agonists and antagonists to determine the receptor subtype mediating dopaminergic mechanisms of action. We demonstrated that dopaminergic transmission at the MoV potently increased motor outflow via the D1-like receptor and facilitated masseter and tensor palatini muscle tone. It is unknown whether endogenous dopamine release on to airway motoneurons influences their activity to regulate muscle tone in natural sleep-wake behaviours. This issue warrants investigation because the neurochemical basis of upper airway motor dysfunction (e.g. obstructive sleep apnea) remains poorly characterized.

The role of dopamine in directly modulating somatic motoneuron excitability and hence muscle tone is unknown. We investigated whether dopamine influences the trigeminal motor pool (MoV) that innervates the masseter and tensor palatini muscles, both of which function to maintain upper airway patency. We hypothesized that dopamine facilitates motor outflow at the MoV. We focally applied apomorphine (nonspecific dopamine receptor agonist) at the MoV in anaesthetized rats. We also applied receptor-specific agonists and antagonists to determine the receptor subtype mediating dopaminergic mechanisms of action. We demonstrated that dopaminergic transmission at the MoV potently increased motor outflow via the D1-like receptor and facilitated masseter and tensor palatini muscle tone. It is unknown whether endogenous dopamine release on to airway motoneurons influences their activity to regulate muscle tone in natural sleep-wake behaviours. This issue warrants investigation because the neurochemical basis of upper airway motor dysfunction (e.g. obstructive sleep apnea) remains poorly characterized.

The digastric muscle of the rabbit consists of a single anterior belly which inserts onto the lower jaw. Horseradish peroxidase was injected into the muscle and into subcutaneous regions overlying the lower jaw to determine the sites of origin of the motor innervation to both the digastric muscle and the platysma muscles. After digastric muscle injection, labelled cells were found in the ipsilateral retrotrigeminal nucleus as well as in the intermediate subnucleus of the main facial nucleus on both sides. Subcutaneous injections produced labelling which was found bilaterally in the intermediate subnucleus and in the ventromedial portion of the medial subnucleus. These results are interpreted in relation to the common embryological origin of these two muscles and their innervation.

The distribution of urotensin-II-immunoreactivity (irU-II) was studied in the rat brainstem and spinal cord with the use of an antiserum against the human urotensin II (U-II) peptide. A population of ventral horn neurons in the spinal cord, hypoglossal nucleus, dorsal motor nucleus of the vagus, facial motor nucleus, nucleus ambiguus, abducens nucleus and trigeminal motor nucleus exhibited irU-II of varying intensities. The number of irU-II motor neurons was higher in the lumbar segments as compared to that of cervical, thoracic and sacral segments. Double-labeling the sections with U-II- and choline acetyltransferase (ChAT)-antisera revealed that nearly all irU-II ventral horn and brainstem neurons were ChAT-positive. The result provides the first immunohistochemical evidence of the presence of irU-II in cholinergic motoneurons of the rat spinal cord and brainstem.