Diphenidol and Vestibular Function&lt;subtitle&gt;A Comparative Study With Chlorpromazine in Rabbits&lt;/subtitle&gt;

Katz, R.

doi:10.1001/archotol.1969.00770020490009

Cited by 4 publications

(2 citation statements)

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“…normalizing effect of antipsychotics in noncatatonic schiz., so drugs unlikely to have obscured group differences. Same variability in drug effects here noted by others (Salerno 1955;Jongkees and Phillipszoon 1960;Jongkees 1961;Lachmann 1961;Eviatar and Goodhill 1968;Katz, Eviatar, and Goodhill 1969;Czech, Nowicki, and Zaleski 1974), possibly due to individual differences in response to dosage (Bergstrom and Koch 1956) and inhibitory effect of drugs on reticular formation mediation of arousal (Bergstrom and Koch 1956;Taniewski 1958); (8) drug status and clinical state confounded in catatonics, but not in earlier studies. Drugs seem to improve clinical condition, which correlates with duration independent of medications.…”

Section: Appendix 1 Studies Of Vestibular Functioning In Adult Schizo...supporting

confidence: 54%

Vestibular Dysfunction and Psychopathology

Levy¹,

Holzman²,

Proctor³

1983

Schizophrenia Bulletin

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A review of the empirical findings linking vestibular response abnormalities to psychopathology, and particularly to schizophrenia, indicates that these data do not unequivocally document the presence of peripheral or central disease of the vestibular system in any patient group. The reasons for this ambiguity include: use of imprecise stimulation techniques, inaccurate measures of responsiveness, unreliable measures of quantification, and the absence of experimental control over extravestibular variables. Future directions for research in this area are discussed, including the localizing information derived from properly conducted tests of the vestibulo-ocular reflex in studies of oculomotor function.

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Section: Appendix 1 Studies Of Vestibular Functioning In Adult Schizo...supporting

confidence: 54%

Vestibular Dysfunction and Psychopathology

Levy¹,

Holzman²,

Proctor³

1983

Schizophrenia Bulletin

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“…2m). Moreover, treatment of mice with the vestibular depressant and anti-vertigo agent difenidol (11 mg kg −1 ) 16 failed to alter the fear of heights in the OHP test (Supplementary Fig. 4k).…”

Section: Vestibular Input Is Dispensable To Fear Of Heightsmentioning

confidence: 97%

A non-image-forming visual circuit mediates the innate fear of heights in male mice

Shang,

Xie,

Feng

et al. 2024

Nat Commun

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The neural basis of fear of heights remains largely unknown. In this study, we investigated the fear response to heights in male mice and observed characteristic aversive behaviors resembling human height vertigo. We identified visual input as a critical factor in mouse reactions to heights, while peripheral vestibular input was found to be nonessential for fear of heights. Unexpectedly, we found that fear of heights in naïve mice does not rely on image-forming visual processing by the primary visual cortex. Instead, a subset of neurons in the ventral lateral geniculate nucleus (vLGN), which connects to the lateral/ventrolateral periaqueductal gray (l/vlPAG), drives the expression of fear associated with heights. Additionally, we observed that a subcortical visual pathway linking the superior colliculus to the lateral posterior thalamic nucleus inhibits the defensive response to height threats. These findings highlight a rapid fear response to height threats through a subcortical visual and defensive pathway from the vLGN to the l/vlPAG.

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A non-image-forming visual circuit mediates the innate fear of heights

Shang

Xie

Wang

et al. 2023

Preprint

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The neural basis of fear of heights remains essentially unknown. We observed mice displaying stereotyped aversive behaviors when encountered height threats, resembling human height vertigo. Visual input plays a crucial role in mouse reactions to heights, which can also be influenced by vestibular input and prior height experiences. Unexpectedly, fear of heights in inexperienced mice does not rely on image-forming visual processing by the primary visual cortex. Instead, a subset of neurons in the ventral lateral geniculate nucleus (vLGN) connecting to the lateral/ventrolateral periaqueductal gray (l/vlPAG) drives the expression of height-related fear. Additionally, a subcortical visual pathway linking the superior colliculus to the lateral posterior thalamic nucleus inhibits the defensive response to height threats. These findings highlight an unconscious fear response to height threats through a rapid subcortical visual and defensive pathway from vLGN to l/vlPAG.One-Sentence SummaryA non-image visual mechanism of fear of heights

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Diphenidol and Vestibular Function<subtitle>A Comparative Study With Chlorpromazine in Rabbits</subtitle>

Cited by 4 publications

References 1 publication

Vestibular Dysfunction and Psychopathology

Vestibular Dysfunction and Psychopathology

A non-image-forming visual circuit mediates the innate fear of heights in male mice

A non-image-forming visual circuit mediates the innate fear of heights

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