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  • Title: Central compensation of vestibular deficits. IV. Responses of lateral vestibular neurons to neck rotation after labyrinth deafferentation.
    Author: Xerri C, Gianni S, Manzoni D, Pompeiano O.
    Journal: J Neurophysiol; 1985 Oct; 54(4):1006-25. PubMed ID: 3877791.
    Abstract:
    The response characteristics of neurons located in the lateral vestibular nucleus (LVN) to neck rotation at 0.026 Hz, 10 degrees peak displacement, have been investigated in precollicular decerebrate cats submitted to ipsilateral acute (aVN) or chronic vestibular neurectomy (cVN). On the whole, 105 units were tested after aVN (i.e., during the first postoperative hours) and 132 units after cVN (i.e., after full compensation of the postural and locomotor deficits). The neurons were histologically located either in the rostroventral (rvLVN) or the dorsocaudal part (dcLVN) of Deiters' nucleus, which are known to project mainly to the cervical and the lumbosacral cord, respectively. Moreover, 55 units in the former group and 66 units in the latter group were identified as vestibulospinal neurons projecting to lumbosacral segments of the spinal cord. The responses of these 237 LVN neurons to the neck input were then compared with those of 120 LVN neurons recorded previously in decerebrate cats with intact labyrinths. Whereas 58.3% of the LVN units recorded in control experiments were responsive to neck rotation, 69.5% of the units were affected by this stimulation at the acute stage of the neurectomy and 74.2% at the chronic stage. This increase in responsive units after aVN and cVN with respect to the controls was found exclusively in the dcLVN. The mean discharge rate of the responsive LVN neurons decreased from 40.7 +/- 48.9 (SD) imp/s in control experiments to 22.1 +/- 15.8 (SD) imp/s after a VN. Similar value was also obtained after cVN [25.0 +/- 17.2 (SD) imp/s], suggesting that compensation of the postural deficits elicited by the vestibular neurectomy results from a redistribution of the excitatory drive within different populations of LVN neurons. Indeed, the relation found in control experiments, i.e., that the faster the conduction velocity of vestibulospinal axons the lower was the unit discharge at rest, was lost after aVN, due to a decrease in resting discharge of the slow units. The mean discharge rate of the slow units, however, recovered after cVN, so that the negative correlation between resting discharge rate and axonal conduction velocity was reestablished. The average gain and sensitivity of the first harmonic response of the LVN neurons to neck rotation recorded after aVN and cVN were comparable to those obtained in preparations with the vestibular nerves intact.(ABSTRACT TRUNCATED AT 400 WORDS)
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