title: The monoaminergic control of gamma motoneurones
Creators: name: Sahal, Anil
Publisher: name: University of Glasgow
Year: 2001
Subjects: subject: Neurosciences
subject: FOS: Clinical medicine

description: 1. The monoamines are known to modulate transmission from group II muscle afferents to gamma-motoneurones in the cat. Noradrenaline has a suppressive effect whereas serotonin facilitates this transmission. The aim of this study was to determine whether gamma-motoneurones are innervated by noradrenergic and serotoninergic neurones. 2. Eight gamma-motoneurones were investigated. These had been identified by their conduction velocity and labelled by ionophoretic microinjection of rhodamine- dextran intracellularly. 50mum thick sagittal sections of spmal cord contaming these gamma-motoneurones were cut and these were exposed to antibodies against serotonin and dopamine beta-hydroxylase (DBH), the final enzyme involved in the conversion of dopamine into noradrenaline. 3. A three-colour confocal laser scanning microscope was used to examine the 50?m thick sections. Optical sections were gathered from the areas where the gamma-motoneurones were identified. These optical sections were analysed to establish any appositions between serotonin- and DBH-immunoreactive fibres. 4. Serotoninergic and noradrenergic varicosities formed appositions with the somata and dendrites of all the gamma-motoneurones. Monoaminergic appositions on dendrites greatly outnumbered those on the somata. The mean densities for serotonin were 1.12 + 0.11 appositions per 100mum on the somata and 0.91 +/- 0.07 per 100?m for dendrites. These data were similar to those reported for a-motonevirones. The density of DBH appositions was consistently lower than for serotonin, with corresponding means 53% and 62% of those for serotonin on the somata and dendrites respectively. 5. For the two best labelled y-motoneurones, the number of appositions on the dendrites was compared to the number of varicosities in a 5mum wide shell around the dendrites. This comparison showed that the number of noradrenergic and serotoninergic appositions was more than ten times greater than would be expected by chance alone. Thus it was concluded that the gamma-motoneurones were innervated by serotoninergic and noradrenergic axons. 6. High doses of potent opiates such as fentanyl are known to be responsible for muscular rigidity. This is particularly dangerous since fentanyl is routinely used as an anaesthetic agent and the rigidity often occurs in the crucial stage just prior to intubation and artificial ventilation. These procedures are much more difficult when muscle rigidity is present. 7. It has been shown that rigidity can be induced in anaesthetised rats by injecting opiates into the locus coeruleus, which is the main source of noradrenaline in the spinal cord. Opiates suppress noradrenergic release. Since noradrenaline has facilitatory effects on alpha-motoneurones, and gamma-motoneurones should be disinhibited, it was argued that gamma-motoneurones may be involved in the mechanism for opiate induced rigidity. 8. It was found that systemic injection of fentanyl into urethane anaesthetised rats produced a surge in the activity of gamma-motoneurones supplying a caudal muscle. This surge preceded any EMG activity, thus suggesting that the excitation of the gamma-motoneurones was secondary to the excitation of the muscle spindles by the gamma-motoneurones. 9. The depressive effect of fentanyl on the respiratory rhythm generator caused apnoea. The surge in the activity of gamma-motoneurones occurred with a latency of about 50 seconds after the onset of apnoea caused by the administration of fentanyl or after stopping the ventilator. 10. It was postulated that the delay before the onset of the gamma-activity was due to the accumulation of CO2 and/or to progressive hypoxia. It was found that the surge in gamma-motoneurone activity could not be induced by the administration of various gas mixtures (hypoxic, hypercapnoeic and hypoxic/hypercapnoeic) to the rat in the presence of fentanyl. Also, if there was some residual rhythmic respiratory effort, the gamma-surge did not occur. This suggested that the tonic activity of afferents normally activated rhythmically during respiration was responsible for the switch to rigidity. However, cutting the vagus bilaterally to abolish the input from lung stretch afferents had no effect on this phenomenon. It is therefore suggested that tonic activity of afferents from receptors in the chest wall and abdomen are important in initiating opiate induced rigidity. A mechanism for this phenomenon involving the locus coeruleus, the raphe nuclei and the periaqueductal grey matter in the brainstem is proposed.