ArticleBandage backfall: Labyrinthine and non-labyrinthine components
References (45)
- et al.
Lateralized effects of monocular training on dendritic branching in adult split-brain rats
Brain Res
(1982) - et al.
Morphine versus haloperidol catalepsy in the rat: a behavioral analysis of postural mechanisms
Brain Res
(1980) - et al.
Vestibular ototoxicity
- et al.
Olfactory nerve projections to the olfactory bulb in rabbit: demonstration by means of a simplified ammoniacal silver degeneration method
Brain Res
(1970) The Basal Ganglia and Posture
(1967)- et al.
Fractionation of postural support mechanisms with combined systemic administration of haloperidol and morphine
Soc Neurosci Abstr
(1983) - et al.
Compensation of labyrinthine lesions: Effects of trigeminal neurotomy on vestibular field potentials
Physiol Behav
(1979) - et al.
Bulbocapnine catalepsy and the grasp reflex
J Pharmacol Exp Ther
(1931) Awakenings
(1976)- et al.
Trigemino-neck reflex: its peripheral and central organization
Trigeminal contribution to the head righting reflex
Physiol Behav
The clinging position of the bulbocapninized cat
Exp Neurol
A propos de la nature de la catalepsie experimentale
Arch Physiol Neerl
Facilitation of maternal transport by Norway rat pups
J Comp Physiol Psychol
Retrograde cellular changes in the mesencephalic trigeminal nucleus in the cat following cerebellar lesions
Acta Morphol Neerl Scand
Fiber projections from the spinal trigeminal nucleus in the cat
J Comp Neurol
Two components in the bandage-backfall reaction
Experimental Catatonia. A General Reaction-Form of the Central Nervous System and its Implication for Human Pathology
Morphine catalepsy as an adaptive reflex state in rats
Behav Neurosci
The behavior of animals in restraint
Behavioral assessment of sodium arsanilate induced vestibular dysfunction in rats
Physiol Psychol
Pimozide, a chemically novel, highly potent and orally long-acting neuroleptic drug. Part 1: The comparative pharmacology of pimozide, haloperidol and chlorpromazine
Arzneimittelforsch
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The neural correlates of navigation beyond the hippocampus
2015, Progress in Brain ResearchCitation Excerpt :Studies found that damaging or inactivating the vestibular system results in a loss of direction-specific discharge in cells recorded from the ADN and postsubiculum (see Clark and Taube, 2012; Shinder and Taube, 2014; Taube, 2007). One study injected sodium arsanilate into the middle ear, which causes degeneration of the neuroepithelium of the vestibular cristae ampullares, maculae utriculi, and cochlea (Kaufman et al., 1992), as well as degeneration of the vestibular nerve in the brainstem (Chen et al., 1986). Not only did the injections lead to a loss of direction-specific firing, but cells also appeared that fired with intermittent bursts (i.e., bursty cells), which were not related to the animal's HD (Stackman and Taube, 1997).
Evaluation of the chemical model of vestibular lesions induced by arsanilate in rats
2012, Toxicology and Applied PharmacologyCitation Excerpt :Based on several studies, it has been postulated that surgical lesions were more selective, destroying the eighth cranial nerve or vestibular sense organ alone, while the chemical lesions were more diffuse and difficult to contain. Among various potential pharmacological agents, sodium arsanilate, an analog of phosphoric acid, remains one of the most commonly used for inducing chemical vestibular lesions (Andersson et al., 1997; Aoki et al., 1996; Chen et al., 1986; Kaufman et al., 1992; Kim et al., 2002; Ossenkopp et al., 1990, 1994; Stackman et al., 2002). According to evidence-based properties of arsanilic acid, it is commonly assumed that transtympanic injection of this drug (range 5 to 30 mg/ear in rodents) not only induces vestibular damage (Anniko and Wersäll, 1977), but also promotes degeneration of the eighth cranial nerve (Andersson et al., 1997), and probably spreads to cause oropharyngeal and brainstem lesions.
Effects of acute hypotension on expression of cFos-like protein in the vestibular nuclei of rats
2003, Brain ResearchCitation Excerpt :The extent to which sodium arsanilate treatment leads to degeneration of the brainstem (e.g., vestibular and cochlear) and cerebellar nuclei has not been fully assessed. Furthermore, histological analyses of the consequences of sodium arsanilate treatment for the vestibular nerve and nuclei have not been performed, although several previous reports have described effects of this type [2,11,21]. Stackman and Taube [38] did not observe any gross damage due to sodium arsanilate treatment in anterior thalamic nuclei using light microscopy.
Rats with lesions of the vestibular system require a visual landmark for spatial navigation
2002, Behavioural Brain ResearchCitation Excerpt :Lesion of the vestibular system was complete within 24–48 h following arsanilate treatment, as judged by a failure of the contact-righting reflex by the lesioned rats [4,36]. The contact-righting test is sensitive to vestibular dysfunction induced both surgically and by trans-tympanic injection of sodium arsanilate [4,17,29,36,39]. The contact-righting test requires placing the rat supine on a tabletop surface and bringing a Plexiglas surface into gentle contact with the ventral surface of the rat's feet.