Positional and directional preponderances in vection

Takeharu Senoo, Takao Sato

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

We examined the biases in vection strength caused by motion direction (temporonasal vs. nasotemporal motion) and position of stimulus presentation (nasal and temporal semi-retinas) to investigate a subcortical contribution to vection. These biases have been identified for optokinetic nystagmus (OKN) and are acknowledged as evidence for a subcortical origin of OKN. In experiments, subjects monocularly observed hemi-field motion stimuli and made magnitude estimations. The results indicated significant directional and positional biases when luminance modulated gratings were used as stimuli. Vection was stronger with nasotemporal motions and nasal retina presentations, but there were no interactions between the two factors. However, these biases disappeared for second-order motion stimuli (contrast modulation), which are presumably processed by the cortex. In addition, when subjects were asked to make subjective ratings of motion impression, there was no significant difference in subjective strength between the stimuli that induced the strongest vection and weakest vection. These results, together, suggest the involvement of the subcortical pathway in vection induction.

Original languageEnglish
Pages (from-to)221-229
Number of pages9
JournalExperimental Brain Research
Volume192
Issue number2
DOIs
Publication statusPublished - Jan 1 2009
Externally publishedYes

Fingerprint

Optokinetic Nystagmus
Nose
Retina
Direction compound

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Positional and directional preponderances in vection. / Senoo, Takeharu; Sato, Takao.

In: Experimental Brain Research, Vol. 192, No. 2, 01.01.2009, p. 221-229.

Research output: Contribution to journalArticle

@article{ae5804d7c42645a79ecc85c7843b13a0,
title = "Positional and directional preponderances in vection",
abstract = "We examined the biases in vection strength caused by motion direction (temporonasal vs. nasotemporal motion) and position of stimulus presentation (nasal and temporal semi-retinas) to investigate a subcortical contribution to vection. These biases have been identified for optokinetic nystagmus (OKN) and are acknowledged as evidence for a subcortical origin of OKN. In experiments, subjects monocularly observed hemi-field motion stimuli and made magnitude estimations. The results indicated significant directional and positional biases when luminance modulated gratings were used as stimuli. Vection was stronger with nasotemporal motions and nasal retina presentations, but there were no interactions between the two factors. However, these biases disappeared for second-order motion stimuli (contrast modulation), which are presumably processed by the cortex. In addition, when subjects were asked to make subjective ratings of motion impression, there was no significant difference in subjective strength between the stimuli that induced the strongest vection and weakest vection. These results, together, suggest the involvement of the subcortical pathway in vection induction.",
author = "Takeharu Senoo and Takao Sato",
year = "2009",
month = "1",
day = "1",
doi = "10.1007/s00221-008-1575-6",
language = "English",
volume = "192",
pages = "221--229",
journal = "Experimental Brain Research",
issn = "0014-4819",
publisher = "Springer Verlag",
number = "2",

}

TY - JOUR

T1 - Positional and directional preponderances in vection

AU - Senoo, Takeharu

AU - Sato, Takao

PY - 2009/1/1

Y1 - 2009/1/1

N2 - We examined the biases in vection strength caused by motion direction (temporonasal vs. nasotemporal motion) and position of stimulus presentation (nasal and temporal semi-retinas) to investigate a subcortical contribution to vection. These biases have been identified for optokinetic nystagmus (OKN) and are acknowledged as evidence for a subcortical origin of OKN. In experiments, subjects monocularly observed hemi-field motion stimuli and made magnitude estimations. The results indicated significant directional and positional biases when luminance modulated gratings were used as stimuli. Vection was stronger with nasotemporal motions and nasal retina presentations, but there were no interactions between the two factors. However, these biases disappeared for second-order motion stimuli (contrast modulation), which are presumably processed by the cortex. In addition, when subjects were asked to make subjective ratings of motion impression, there was no significant difference in subjective strength between the stimuli that induced the strongest vection and weakest vection. These results, together, suggest the involvement of the subcortical pathway in vection induction.

AB - We examined the biases in vection strength caused by motion direction (temporonasal vs. nasotemporal motion) and position of stimulus presentation (nasal and temporal semi-retinas) to investigate a subcortical contribution to vection. These biases have been identified for optokinetic nystagmus (OKN) and are acknowledged as evidence for a subcortical origin of OKN. In experiments, subjects monocularly observed hemi-field motion stimuli and made magnitude estimations. The results indicated significant directional and positional biases when luminance modulated gratings were used as stimuli. Vection was stronger with nasotemporal motions and nasal retina presentations, but there were no interactions between the two factors. However, these biases disappeared for second-order motion stimuli (contrast modulation), which are presumably processed by the cortex. In addition, when subjects were asked to make subjective ratings of motion impression, there was no significant difference in subjective strength between the stimuli that induced the strongest vection and weakest vection. These results, together, suggest the involvement of the subcortical pathway in vection induction.

UR - http://www.scopus.com/inward/record.url?scp=56349135791&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=56349135791&partnerID=8YFLogxK

U2 - 10.1007/s00221-008-1575-6

DO - 10.1007/s00221-008-1575-6

M3 - Article

VL - 192

SP - 221

EP - 229

JO - Experimental Brain Research

JF - Experimental Brain Research

SN - 0014-4819

IS - 2

ER -