The Lateral Reticular Nucleus. Role in Vestibular Compensation

Abstract

These experiments were performed to verify an assumption resulting from previous researches. It was, in fact, observed that compensation of defects provoked by unilateral lesion of the labyrinth could be impaired by removal of spinal afferents. This spinal decompensation was followed by the reappearance of all the symptoms elicited by previous vestibular deafferentation (Azzena 1969). Furthermore, the balance of electrical activity between the vestibular nuclear complexes of both sides was upset by spinal decompensation and was found to be similar to that recorded in the acute stage of unilateral labyrinthectomy (Azzena et al. 1976, 1977). Thus, the release of vestibular symptoms depended upon the different level of excitability of the vestibular nuclei. According to these results, the vestibular compensation could be considered as a substitution process in which the spinal cord is involved. Since the effects of unilateral lesion of the labyrinth result in a dramatic alteration of postural tone and of oculomotor control, it was assumed that the role of the spinal cord in compensation could take place through the influence of the spino-reticular pathways. In fact, the ascending spino-reticular neurons must be deeply modified by the postural asymmetries which follow unilateral vestibular deafferentation. Since these neurons receive signals arising from the bilateral cutaneous and high threshold afferents (components of flexor reflex afferents, FRA; Eccles and Lundberg 1959; Grant et al. 1966; Lundberg and Oscarsson 1962; Oscarsson 1973; Oscarsson and Rosén 1966), the lesion of one labyrinth should be followed by an asymmetrical projection on the spino-reticular neurons. Furthermore, the same neurons are modulated by descending signals from ipsilateral Deiters’ nucleus and contralateral somatosensory cortex (Brodai et al. 1967; Clendenin et al. 1974; Coulter et al. 1974, 1976; Grillner et al. 1968; Hoshino and Pompeiano 1977; Künzle and Wiesendanger 1974; Kuypers 1958a,b,c; Pompeiano 1975, 1977; Pompeiano and Hoshino 1977; Rosén and Scheid 1973b).