Effects of carbon monoxide on responding under a progressive ratio schedule in rats.
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Biomedical subjects
Publications and source records attributed to W H Merigan.
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Four rats were trained under a fixed-consecutive-number (FCN) schedule to make sequences of 20 or more consecutive responses on one lever followed by a single response on a second lever. When performance was stable, they were exposed to 200, 400, and 600 parts-per-million (PPM) carbon monoxide (CO) for either 30 or 60 min before and during a 45-min session. Decreases in response rate at CO levels as low as 200 ppm were due to both decreased local response rate and extended pauses. A lowered percentage of reinforcement, due to decreases in response sequence length, was also found at CO levels as low as 200 ppm. This decreased sequence length may reflect effects of CO on response rate, or a disruption of discriminative aspects of FCN schedule performance.
Pigeons were exposed to multiple variable-interval 2-min variable-interval 2-min schedules of food presentation in which relative duration of food presentation was manipulated. When components alternated every 5 sec and were scheduled on separate response keys, relative response rates closely matched relative reinforcement duration in three of four pigeons. On the other hand, relative response rates were insensitive to relative reinforcement duration when components scheduled on a single response key alternated every 5 sec, and when components scheduled on separate response keys alternated every 2 min. Thus, both rapid alternation and spatial separation of components were necessary to produce approximate matching of relative responding to relative reinforcement duration. This finding contrasts with previous findings that only rapid component alternation is necessary for matching when relative rate of reinforcement is manipulated.
Ibotenic acid lesions were made in four macaque monkeys in a region of cortical area V4 that corresponds to the lower quadrant of one hemifield. For visual testing, fixation locus was monitored with scleral search coils and controlled behaviorally to place test stimuli either in the lesioned quadrant or in a control location in the opposite hemifield. Some basic visual capacities were slightly altered by the lesions; there was a two-fold reduction of luminance contrast sensitivity as well as red-green chromatic contrast sensitivity, both tested with stationary gratings. On the other hand, little or no loss was found when contrast sensitivity for detection or direction discrimination was tested with 10-Hz drifting gratings nor was there a reliable change in visual acuity. Hue and luminance matching were tested with a spatially more complex matching-to-sample task, but monkeys could not learn this task in the visual field locus of a V4 lesion. If previously trained at this locus, performance was not affected by the lesion. In contrast to the small effects on basic visual capabilities, performance on two form discrimination tasks was devastated by V4 lesions. The first involved discriminating the orientation of colinear groups of dots on a background of randomly placed dots. The second involved discriminating the orientation of a group of three line segments surrounded by differently oriented line segments. Some selectivity of the deficits for form discrimination was shown by the lack of an effect of the lesions on a global motion discrimination. These results show that while V4 lesions cause only slight disruptions of basic visual capacities, they profoundly disrupt form discriminations.
This study examined the question of which features of a complex grouping discrimination make it vulnerable to permanent elimination by V4 lesions. We first verified that the line element grouping discrimination, which we previously reported to be devastated by V4 lesions, was similarly affected in the monkeys of this study. The permanence of the deficit was established by mapping its visual field distribution and then testing this discrimination for an extended period at a locus on the border of the deficit. Also, a staircase procedure was used to provide the monkey with within session instruction in the grouping discrimination, but this did not improve V4 lesion performance. Grouping was then compared with several discriminations that shared some features with it, but which were found not to be permanently eliminated by V4 lesions. This comparison suggested that grouping (rather than segmentation or response to a single element) was one feature that made the discrimination vulnerable, a second was the similarity in shape of the texture elements to be grouped. Finally, we tested visual crowding, a property of peripheral vision that is thought to reflect neuronal interactions early in visual cortex, possibly in area V1, and found no effect of V4 lesions. A control experiment with human observers tested whether the elimination of grouping by V4 lesions might be due to an alteration of attention, but found no evidence to support this hypothesis. These results show that severe disruption of texture discriminations by V4 lesions depends on both the nature of the discrimination and the type of texture elements involved, but does not necessarily involve the disruption of attention.
The role of cortical area V4 in complex shape discriminations was studied by testing the effects of V4 lesions in macaques on the ability to visually discriminate between images of three-dimensional (3D) objects from different viewpoints. Stimuli were presented in pairs in the lower left or lower right visual field quadrants about 4 deg from the fovea, and the monkeys judged on each trial whether the two views were of the same or of different objects. Object similarity was varied to determine a threshold shape difference. V4 lesions caused profound, retinotopic, and apparently permanent disruptions of discrimination, regardless of whether the images represented single or multiple viewpoints. In V4 lesioned portions of the visual field, monkeys could discriminate objects only when they differed much more grossly in shape than was true in control locations. These effects of the lesion were virtually identical for discriminations that had been learned before lesions were placed and for those learned afterwards. As in previous studies, V4 lesions elevated contrast thresholds by approximately a factor of two, but control observations showed that this was not the basis of the disruption of shape discrimination. Manipulation of cues to shape showed that in control locations, monkeys maintained excellent shape discrimination despite a variety of stimulus alterations, whereas in V4 lesioned areas their performance was easily disrupted. This finding suggests that V4 may support visual shape discriminations by facilitating the use of multiple visual cues. However, the fact that single-viewpoint and multiple-viewpoint discriminations were similarly affected indicates that the disruption was not specific to 3D shape discrimination, but may apply to a variety of subtle discriminations.
We examined the effect of bilateral ibotenic acid lesions, aimed at areas MT/MST in three macaques, on their perception of motion. The medial boundary of the lesions in the three monkeys was near the dorsal end of the STS, but the lesions extended different lengths ventrally along the STS. The lesions extended the shortest distance ventrally monkeys 1 and 2, covering most of MST but possibly sparing a portion of lateral MT. That in monkey 3 damaged all of MT and MST bilaterally and extended through most of FST. All three lesions caused a temporary disruption, followed by at least partial recovery, of most motion thresholds. Permanent effects of the lesions on visual sensitivity were graded with lesion extent. Contrast sensitivity for detecting low-spatial-frequency (1 cycle/degree) drifting gratings over a wide range of drift rates, as well as for identifying their direction of motion, was slightly affected only in monkey 3. Only monkeys 2 and 3 showed a deficit in discriminating stimulus speed, and the size of the loss was two- to fourfold. Discrimination of opposite directions of dot pattern motion, which required integration of local motion signals, was mildly affected in monkeys 2 and 3, and not affected in monkey 1. However, addition of directional noise to this discrimination caused the performance of all monkeys to be permanently disrupted, especially that of monkeys 2 and 3. Finally, direction difference thresholds were elevated by a factor of 2-4 after the lesions in all three monkeys. Many of these deficits were more pronounced during the first 2 months of testing following the lesion. Thus, our results demonstrate that areas within dorsal STS make an important contribution to the performance of various motion perception tasks including the discrimination of small differences in direction and speed, and the perception of global motion in the presence of directional noise. The residual motion perception, even in the monkey with virtually complete removal of areas MT/MST, may suggest either that these tasks are normally mediated in part by cortical areas outside of areas MT and MST, or that the disrupted functions were partially assumed by other cortical areas after lesions.
Visual system consequences of exposure to methylmercury were studied in six adult, macaque monkeys. Visual field measures, visual thresholds, and morphological examination were used to determine the nature and possible reversibility of alterations in vision. Visual field constriction (especially in the inferior-nasal field) was an early and apparently reversible indicator of methylmercury intoxication. Such a field loss was found in the absence of either visual threshold changes or morphologic alterations in visual cortex. More severe poisoning resulted in persistent field constriction, disruption of visual thresholds, and death. A single monkey showed a permanent, bilateral concentric constriction of visual fields. The locus of visual cortex pathology in this monkey corresponded to the projection of the peripheral visual field.