Central compensation of vestibular deficits. III. Response characteristics of lateral vestibular neurons to roll tilt after contralateral labyrinth deafferentation.
The responses of lateral vestibular nucleus (LVN) neurons to stimulation of macular labyrinth receptors have been investigated in precollicular decerebrate cats after contralateral acute vestibular neurectomy (aVN). On the whole, 78 LVN neurons were tested during slow sinusoidal tilt of the animal at the standard parameters (0.026 Hz, 10 degrees peak displacement). The neurons were located in both the rostroventral (rvLVN) and the dorsocaudal parts (dcLVN) of Deiters' nucleus, which project mainly to the cervical and the lumbosacral cord, respectively. After contralateral aVN, the proportions of responsive units in rvLVN and dcLVN (100% and 75.4%, respectively) were similar to those obtained in control experiments with intact labyrinths. However, the mean discharge rate of the responsive units slightly decreased with respect to the value obtained in control experiments, the decrease being more prominent within the rvLVN. The average sensitivity (and to a lesser extent the gain) of responses of rvLVN neurons to the labyrinth input was almost twice that of the dcLVN units in preparations with the vestibular nerves intact; these regional differences disappeared after contralateral aVN, particularly due to a decrease in gain and sensitivity of responses in the rvLVN. The proportion of LVN neurons that were maximally excited by animal position increased from 74.0% in the control experiments to 82.8%. However, while in control experiments the proportion of units excited during side-down tilt was twice as high as that of the units excited by side-up tilt, the opposite occurred after contralateral aVN; this finding affected particularly the dcLVN. In addition the average phase lead of responses relative to the extreme animal displacements slightly decreased from +12.3 degrees in control experiments to +9.4 degrees. Among the LVN neurons recorded after contralateral aVN, 35 were antidromically activated by stimulating the spinal cord at T12 L1, while 43 units were not activated. The relation found in control experiments, i.e., that the faster the conduction velocity of vestibulospinal axon the lower was the unit discharge at rest, was lost after contralateral aVN, due to a decrease in resting discharge rate of the slow neurons. This finding, coupled with the observation that slow and fast units did not show any difference in their response gain to tilt, explains why the positive correlation between axonal conduction velocity and response sensitivity occurring in control experiments was lost after contralateral aVN.(ABSTRACT TRUNCATED AT 400 WORDS)
D000222:Adaptation, Physiological; D000818:Animals; D002415:Cats; D003655:Decerebrate State / Q000503:physiopathology; D004525:Efferent Pathways / Q000503:physiopathology; D007759:Labyrinth Diseases / Q000503:physiopathology; D009431:Neural Conduction; D011187:Posture; D013116:Spinal Cord / Q000503:physiopathology; D014726:Vestibular Nuclei / Q000503:physiopathology*; D003689:Vestibular Nucleus, Lateral / Q000502:physiology; D014722:Vestibule, Labyrinth