Chapter 7 The role of Renshaw cells in the dynamic control of posture during vestibulospinal reflexes

Abstract

Contraction of limb extensors during side-down tilt of the animal can be attributed to an increased discharge of lateral VS neurons which exert an excitatory influence on ipsilateral extensor motoneurons (α response). However, in addition to these neurons there are other neuronal systems, such as the CS and the medullary inhibitory RS neurons which also respond to animal tilt, but with a predominant response pattern characterized by a reduced discharge during side-down tilt (β response). This finding is surprising since the CS projection, which originates from the NE-containing LC neurons, is inhibitory on R cells linked with limb extensor (and flexor) motoneurons, while the medullary RS projection, which is driven presumably by cholinergic and cholinoceptive neurons located in the dorsal pRF, is excitatory on them. Experiments were performed in precollicular decerebrate cats to investigate the relative influence that the CS, as well as the RS, neurons exert on R cells coupled with limb extensor motoneurons in the following experimental conditions: (1) during the state of postural activity in which the LC neurons showed a steady discharge while the pRF neurons, as well as the related medullary inhibitory RS neurons, fired at a very low rate; in this instance the gain of the VS reflexes was quite low; and (2) during episodes of reduced postural activity following systemic administration of an anticholinesterase (0.05–0.10 mg/ kg eserine sulphate), in which the discharge rate of LC neurons decreased, while that of the pRF neurons and the related medullary inhibitory RS neurons increased; in this instance the gain of the VS reflexes was greatly enhanced. In particular, the activity of R cells monosynaptically linked with gas-trocnemius-soleus motoneurons (GS R cells) was tested both in the animal at rest as well as during head rotation (at 0.026–0.15 Hz, ± 10°) performed after bilateral neck deafferentation, thus leading to sinusoidal stimulation of labyrinth receptors. In control animals at rest the GS R cells were silent or fired at a low rate; moreover, the same units were either unresponsive or displayed only small-amplitude α responses to labyrinth stimulation. These responses were attributed to the fact that during side-down head rotation the increased discharge of VS neurons activated the GS motoneurons and, through their recurrent collaterals, the related R cells. However, the decrease in firing rate of the CS neurons for the same direction of head rotation would reduce the inhibitory influence that these noradrenergic neurons exert on the GS R cells, thus enhancing the functional coupling of these units with their own extensor motoneurons. This would explain why the response gain of hindlimb extensors to labyrinth stimulation was negligible or absent in these preparations. After systemic injection of the anticholinesterase, leading to an increased discharge of cholinoceptive pRF neurons and the related medullary RS neurons, the GS R cells increased their firing rate in the animal at rest; however, all the R cells which prior to the injection were either unresponsive or showed an a response to head rotation, now showed a β response for the same parameters of labyrinth stimulation. In particular, a reduced discharge of the GS R cells occurred during side-down head rotation, as shown for the majority of the RS neurons. It appears, therefore, that the same R cells which in the control situation responded to the excitatory VS volleys acting through the GS motoneurons were now decoupled from their input motoneurons and underwent the most efficient control of the RS pathway. The reduced discharge of the GS R cells during side-down head rotation would lead to disinhibition of limb extensor motoneurons, thus enhancing the response gain of the corresponding muscle to labyrinth stimulation. The R cells could then act as a variable gain-regulator at moto-neuronal level during the VS reflexes.