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  • Author or Editor: G. Raffai x
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Aims

Labyrinthectomized rats are suitable models to test consequences of vestibular lesion and are widely used to study neural plasticity. We describe a combined microsurgical–chemical technique that can be routinely performed with minimum damage.

Methods

Caudal leaflet of the parotis is elevated. The tendinous fascia covering the bulla is opened frontally from the sternomastoid muscle’s tendon while sparing facial nerve branches. A 4 mm diameter hole is drilled into the bulla’s hind lower lateral wall to open the common (in rodents) mastoid-tympanic cavity. The cochlear crista (promontory) at the lower posterior part of its medial wall is identified as a bony prominence. A 1 mm diameter hole is drilled into its lower part. The perilymphatic/endolymphatic fluids with tissue debris of the Corti organ are suctioned. Ethanol is injected into the hole. Finally, 10 µL of sodium arsenite solution (50 µM/mL) is pumped into the labyrinth and left in place for 15 min. Simple closure in two layers (fascia and skin) is sufficient.

Results and conclusion

All rats had neurological symptoms specific for labyrinthectomy (muscle tone, body position, rotatory movements, nystagmus, central deafness). Otherwise, their behavior was unaffected, drinking and eating normally. After a few days, they learned to balance relying on visual and somatic stimuli (neuroplasticity).

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Circumferential stretch due to increases in pressure induces vascular smooth muscle cell depolarization and contraction known as the myogenic response. The aim of this study was to determine the in vivoeffects of axial-longitudinal stretch of the rat saphenous artery (SA) on smooth muscle membrane potential (Em) and on external diameter. Consecutive elongations of the SA were carried out from resting length (L0) in 10% increments up to 140% L0while changes in membrane potential and diameter were determined in intact and de-endothelized vessels. Axial stretching resulted in a small initial depolarization at 120% of L0followed by a progressive 20 to 33% hyperpolarizaion of vascular smooth muscle between 130% and 140% of L0. At 140%, an average maximal 10.6 mV reversible hyperpolarization was measured compared to –41.2±0.49 mV Em at 100% L0. De-endothelialization completely eliminated the hyperpolarization to axial stretching and augmented the reduction of diameter beyond 120% L0. These results indicate that arteries have a mechanism to protect them from vasospasm that could otherwise occur with movements of the extremities.

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