Search

Destruction of the inner ear in rats for medical research has been performed since 1936. Nevertheless, descriptions of the technique used and clinical analysis are poor and often involve coagulation of the stapedial artery. We suggest a description of a surgical ventrolateral approach to labyrinthectomy in rats, with preservation of the stapedial artery. Methods: Twenty-five Wistar rats were operated on via a right ventrolateral approach to the bulla, followed by labyrinthectomy with preservation of the stapedial artery. Clinical observation and tests were carried out from the time of the surgery until day one. Twenty-four hours after the surgery on the right side, the same surgery was performed on the left side, followed by clinical observation. Twenty-five other rats were used as controls, with sham surgery. Histologic analysis of the vestibular nerve with silver staining was performed in six rats 3 or 7 days after the labyrinthectomy. Results: The ventrolateral approach made it possible to reach the middle- and inner-ear with preservation of nervous and vascular elements such as the facial nerve and stapedial artery. Unilateral labyrinthectomy induced ocular skew deviation, head torsion and limb asymmetry. Dynamic signs were first rolling, then rotation, which increased considerably during tail suspension. Bilateral labyrinthectomy produces instability with major body oscillation. Animals show head and neck dorsiflexion with limb extension, sometimes followed by fast backward walking. Conclusion: The ventrolateral approach is an efficient technique for surgical labyrinthectomy with stapedial artery preservation. Clinical analysis shows a wide range of signs to evaluate the functional destruction of the vestibular organ. [ABSTRACT FROM AUTHOR]

Abstract: Neural control circuits that coordinate the motor activity of the diaphragm (DIA) and the geniohyoid muscle (GH) are potentially involved in pathological conditions such as various forms of sleep apnea. Here we investigated a differential role of the raphe magnus (RMg), pallidus (RPa) and the obscurus (ROb) nuclei in the neural control of DIA and GH muscle activity in rats under volatile anesthesia. In order to characterize a topographical organization of the raphe nuclei we analyzed changes in DIA and GH during high-frequency stimulation (HFS, 10–130Hz, 60μs pulse width, 40–160μA, 30s). HFS of the RMg and the ROb induced apnea, in the latter case apnea was associated with massive tonic discharge in the GH. By contrast, HFS of the RPa induced tachypnea. At caudal stimulation sites the tachypnea was accompanied by tonic DIA activity and cessation of GH. These data suggest a differential distribution of inhibitory and excitatory drives of DIA and GH muscles within distinct raphe nuclei. [Copyright &y& Elsevier]

It is now well established that vestibular information plays an important role in spatial memory processes. Although vestibular lesions induce anxiety in humans, this finding remains controversial in rodents. However, it is possible that anxiety-related behavior is associated with spatial memory impairments after vestibular lesions. We aimed to evaluate anxiety-like behavior and the effect of an anxiolytic treatment during a complex spatial memory task in a rat model of compensated bilateral vestibular lesions. Adult rats were divided into four groups, with or without vestibular lesions and, treated or untreated by diazepam. The vestibular lesion was performed by transtympanic injection of arsanilate and compared to transtympanic saline injection. Diazepam or saline was administered 1 h before each test or learning session. Vestibular-lesioned rats exhibited anxiety-like behavior which was decreased with diazepam. Spatial memory performance was similar in control-treated and untreated groups, suggesting no effect on memory at the dose of diazepam used. Spatial memory performances were not modified by anxiolytic drug treatment in vestibular-lesioned rats compared to vestibular-lesioned rats without drug treatment. We conclude that bilateral vestibular lesions in rats induced anxiety-like behavior which was unrelated to spatial memory impairment and was probably specifically related to the loss of vestibular information. [ABSTRACT FROM AUTHOR]

Abstract: Several animal models of vestibular deficits that mimic the human pathology phenotype have previously been developed to correlate the degree of vestibular injury to cognate vestibular deficits in a time-dependent manner. Sodium arsanilate is one of the most commonly used substances for chemical vestibular lesioning, but it is not well described in the literature. In the present study, we used histological and functional approaches to conduct a detailed exploration of the model of vestibular lesions induced by transtympanic injection of sodium arsanilate in rats. The arsanilate-induced damage was restricted to the vestibular sensory organs without affecting the external ear, the oropharynx, or Scarpa''s ganglion. This finding strongly supports the absence of diffusion of arsanilate into the external ear or Eustachian tubes, or through the eighth cranial nerve sheath leading to the brainstem. One of the striking observations of the present study is the complete restructuring of the sensory epithelia into a non sensory epithelial monolayer observed at 3months after arsanilate application. This atrophy resembles the monolayer epithelia observed postmortem in the vestibular epithelia of patients with a history of lesioned vestibular deficits such as labyrinthectomy, antibiotic treatment, vestibular neuritis, or Ménière''s disease. In cases of Ménière''s disease, aminoglycosides, and platinum-based chemotherapy, vestibular hair cells are destroyed, regardless of the physiopathological process, as reproduced with the arsanilate model of vestibular lesion. These observations, together with those presented in this study of arsanilate vestibular toxicity, suggest that this atrophy process relies on a common mechanism of degeneration of the sensory epithelia. [Copyright &y& Elsevier]