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Role of the Cerebral Cortex on Vestibular Compensation Following
Unilateral Labyrinthectomy in Rats
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Hyun Kwang Ryoo, Seung Bum Yang, Min Sun Kim, Byung Rim Park
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Res Vestib Sci. 2015;14(3):75-82.
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 Abstract
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- Objective: The cerebral cortex can modulate vestibular functions through direct
control of neuronal activities in the vestibular nuclei. The purpose of this study
was to investigate the effect of unilateral cortical lesion or cortical stimulation
on static vestibular symptoms and vestibular nuclear activities at the acute stage
of vestibular compensation following unilateral labyrinthectomy (UL) in rats.
Methods
The photothrombic ischemic injury using rose bengal was induced in
the primary motor cortex or primary sensory cortex, and electrical stimulation
was applied to the primary motor cortex, primary sensory cortex, or sencondary
sensory cortex, respectively, in unilateral labyrinthectomized rats. Static vestibular
symptoms including ocular movement and postural deficits, and expression of
c-Fos protein in the medial vestibular nucleus (MVN) were measured.
Results
Lesion of the motor cortex produced a marked postural deficit with
paralytic weakness in the hindlimb contralateral to UL. Number of spontaneous
nystagmus in animals receiving cortical lesion was significantly increased 2, 6,
and 12 hours after UL compared with animals being UL only. Lesion of the
primary motor cortex or stimulation of the S2 sensory cortex decreased expression
of c-Fos protein in MVN following UL compared with UL only group. Electrical
stimulation of S2 sensory areas caused significant reduction of static vestibular
symptoms and decreased expression of c-Fos protein in MVN 24 hours following UL.
Conclusion
The present results suggest that cerebral cortex involves in recovery
of static vestibular symptoms during vestibular compensation following UL.
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