Korean J Physiol Pharmacol.
1997 Jun;1(3):263-273.
Effects of electrical stimulation of the vestibular system on neuronal
activity of the ipsilateral medial vestibular nuclei following
unilateral labyrinthectomy in rats
- Affiliations
-
- 1Department of Physiology, Wonkwang University, School of Medicine, Iksan 570-749, Korea.
- 2Medicinal Resources Research Center of Wonkwang University, Iksan 570-749, Korea.
Abstract
-
The purpose of this study was to evaluate the effects of electrical
stimulation on vestibular compensation following ULX in rats.
Electrical stimulation (ES) with square pulse (100 ~ 300 uA, 1.0
ms, 100 Hz) was applied to ampullary portion bilaterally for 6 and 24
hours in rats receiving ULX. After ES, animals that showed the recovery
of vestibular symptoms by counting and comparing the number of
spontaneous nystagmus were selected for recording resting activity of
type I, II neurons in the medial vestibular nuclei (MVN) of the
lesioned side. And then the dynamic neuronal activities were recorded
during sinusoidal rotation at a frequency of 0.1 Hz and 0.2 Hz. The
number of spontaneous nystagmus was significantly different 24 hours (p< 0.01, n = 10), but not 6 hours after ULX+ES. As reported by others,
the great reduction of resting activity only in the type I neurons
ipsilateral to lesioned side was observed 6, 24 hours after ULX
compared to that of intact labyrinthine animal. However, the
significant elevation (p < 0.01) of type I and reduction (p < 0.01)
of type II neuronal activity were seen 24 hours after ULX+ES.
Interestingly, gain, expressed as maximum neuronal
activity(spikes/sec)/maximum rotational velocity (deg/sec), was
increased in type I cells and decreased in type II cells 24 hours after
ULX+ES in response to sinusoidal rotation at frequencies of both 0.1 Hz
and 0.2 Hz. This result suggests that accompanying the behavioral
recovery, the electrical stimulation after ULX has beneficial effects
on vestibular compensation, especially static symptoms (spontaneous
nystagmus), by enhancing resting activity of type I neurons and
reducing that of type II neurons.