The Role of Visual Complexity in Affective Reactions to Webpages: Subjective, Eye Movement, and Cardiovascular Responses

2011 ◽  
Vol 2 (4) ◽  
pp. 230-236 ◽  
Author(s):  
Alexandre Tuch ◽  
Sylvia Kreibig ◽  
Sandra Roth ◽  
Javier Bargas-Avila ◽  
Klaus Opwis ◽  
...  
2014 ◽  
Author(s):  
Molly Ann Metz ◽  
Heidi Kane ◽  
Thery Prok ◽  
Christena Cleveland ◽  
Nancy Collins

2007 ◽  
Author(s):  
Enrico Rubaltelli ◽  
Giacomo Pasini ◽  
Rino Rumiati ◽  
Paul Slovic

2009 ◽  
Vol 101 (2) ◽  
pp. 934-947 ◽  
Author(s):  
Masafumi Ohki ◽  
Hiromasa Kitazawa ◽  
Takahito Hiramatsu ◽  
Kimitake Kaga ◽  
Taiko Kitamura ◽  
...  

The anatomical connection between the frontal eye field and the cerebellar hemispheric lobule VII (H-VII) suggests a potential role of the hemisphere in voluntary eye movement control. To reveal the involvement of the hemisphere in smooth pursuit and saccade control, we made a unilateral lesion around H-VII and examined its effects in three Macaca fuscata that were trained to pursue visually a small target. To the step (3°)-ramp (5–20°/s) target motion, the monkeys usually showed an initial pursuit eye movement at a latency of 80–140 ms and a small catch-up saccade at 140–220 ms that was followed by a postsaccadic pursuit eye movement that roughly matched the ramp target velocity. After unilateral cerebellar hemispheric lesioning, the initial pursuit eye movements were impaired, and the velocities of the postsaccadic pursuit eye movements decreased. The onsets of 5° visually guided saccades to the stationary target were delayed, and their amplitudes showed a tendency of increased trial-to-trial variability but never became hypo- or hypermetric. Similar tendencies were observed in the onsets and amplitudes of catch-up saccades. The adaptation of open-loop smooth pursuit velocity, tested by a step increase in target velocity for a brief period, was impaired. These lesion effects were recognized in all directions, particularly in the ipsiversive direction. A recovery was observed at 4 wk postlesion for some of these lesion effects. These results suggest that the cerebellar hemispheric region around lobule VII is involved in the control of smooth pursuit and saccadic eye movements.


Perception ◽  
1972 ◽  
Vol 1 (2) ◽  
pp. 167-175 ◽  
Author(s):  
Nicole Lesèvre ◽  
A Rémond

Experiments are reported the aim of which was to elucidate the cause of each of the components of the lambda response, and particularly to evaluate the role of ‘on’ and ‘off’ visual effects which appear at various times during the oculomotor process and also the possible influence of non-visual mechanisms. Eight subjects with normal sight were studied under the following conditions: (i) horizontal eye movements of 12° were guided by fixation points placed on a dimly-lit uniform black field of 20°; a checkerboard of 6° aperture was placed in this field so as to be integrated into the oculomotor process at different times—at the beginning, during and at the end of the eye movement; (ii) successive horizontal eye movements of 3°, 7° and 11° scanned a checkerboard of 20°, each square of which had a 40′ aperture; (iii) the checkerboard was moved with an amplitude and period similar to those of the eye movements in (ii), but this time with gaze fixed. Horizontal and vertical movements of both eyes were recorded with an EOG. An EEG of the parieto-occipital regions was obtained using eight linked bipolar derivations in line on two montages, median longitudinal and right-left transverse. The EEG and EOG data were digitalized and a numerical programme of waveform recognition was used to identify the beginning of the saccade which triggers the averaging out of the EEG before (100 ms) and after (500 ms) the eye movement. A discussion of the results, taking into account the latency of the different components and their reinforcements or inhibition depending on experimental conditions, suggests that the two initial components of lambda response (including the initial portion of the classical lambda wave) might be due to visual effects (‘off effect’) that arise at the start of the movement or slightly before it at the time that the saccadic suppression begins. The later components could be attributed to visual effects brought into play towards the end of the movement (‘on effect’), when perception becomes normal again. It is, however, difficult to explain some of the results related to the amplitude of lambda components without bringing in a mechanism of non-visual origin (corollary discharge).


1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


1999 ◽  
Vol 276 (1) ◽  
pp. H63-H70 ◽  
Author(s):  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.


1994 ◽  
Vol 266 (2) ◽  
pp. R496-R502 ◽  
Author(s):  
A. S. Haibara ◽  
W. A. Saad ◽  
J. V. Menani ◽  
L. A. Camargo ◽  
A. Renzi

In this study we investigated the influence of electrolytic lesion or of opioid agonist injections into the lateral hypothalamus (LH) on the dipsogenic, natriuretic, kaliuretic, antidiuretic, pressor, and bradycardiac effects of cholinergic stimulation of the medial septal area (MSA) in rats. Sham- and LH-lesioned male Holtzman rats received a stainless steel cannula implanted into the LH. Other groups of rats had cannulas implanted simultaneously into the MSA and LH. Carbachol (2 nmol) injection into the MSA induced water intake, pressor, and bradycardic responses. LH lesion reduced all of these effects (1-3 and 15-18 days). Previous injection of synthetic opiate agonist, FK-33824 (100 ng), into the LH reduced the water intake, natriuresis, kaliuresis, and pressor responses induced by carbachol injected into the MSA. These data show that both electrolytic lesion or injection of an opiate agonist in the LH reduces the fluid-electrolyte and cardiovascular responses to cholinergic activation of the MSA. The involvement of LH with central excitatory and inhibitory mechanisms related to fluid-electrolytic and cardiovascular control is suggested.


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