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PubMed1981

Inhibition, disinhibition, and summation among orientation detectors in human vision.

A vertical test line viewed together with an oblique inducing line appears to be tilted in the opposite direction (orientation contrast); a similar effect results from adapting to an oblique line before presenting the test line (tilt after-effect). The error in perceived orientation caused by a clockwise tilted inducing line may be partially cancelled by a second clockwise tilted inducing line; likewise, adapting to a configuration of two clockwise orientations gives weaker tilt after-effects than adapting to the more effective of the two orientations alone. The angular functions of these "disinhibitory" effects mirror the angular functions of the principal effects. However, combining tilt after-effect and simultaneous contrast in a disinhibition design by having the subject first adapt to a clockwise orientation and then presenting the test line together with a clockwise inducing line results in partial summation rather than disinhibition. The results are consistent with Carpenter's and Blakemore's (1973) hypothesis that orientation contrast and the tilt after-effect are manifestations of cortical inhibition in a network of inhibitory, recurrent lateral connections between cortical orientation detectors. After-effects must be due to prolonged inhibition, probably caused by a sensitivity change in previously inhibited detectors.

Discrimination Learning↗
PubMed1994

The effects of adaptation to visual stimuli on the velocity of subsequent ocular following responses.

We examined the effect of prior adaptation to moving and flickering stimuli on the velocity of subsequent ocular following responses in man. Experiments consisted of two phases: an adaptation phase in which moving or flickering stimuli were presented while the eyes fixated a small spot and a test phase in which ocular following responses were free to occur. The effects resulting from prior adaptation were characterized by determining the mean initial eye velocities in the period 200-500 ms after the onset of the test stimulus. It was found that 8 s of prior exposure to a grating pattern moving at between 1.5 and 4 cycles.s-1 significantly reduced initial eye velocities in all subjects. Prior exposure to a flickering stimulus (temporal frequency 3.2 cycles.s-1) also attenuated the velocities of initial eye movements, but to a far lesser extent. These results suggest that a motion-dependent and a weaker flicker-dependent process have an adaptive influence on the generation of ocular following responses. Initial eye velocities were measured as a function of the contrast of the prior adapting gratings. The velocities were found to decrease with increasing adapting contrast. The reductions in eye velocity were well described by a decaying exponential function. The motion-dependent adaptive effect showed significant inter-ocular transfer and had the same temporal tuning when transferred (i.e. optimum adaptation at between 1.5 and 4 cycles.s-1). The flicker-dependent effect did not show inter-ocular transfer. There is a distinct similarity between the adaptive process that causes attenuation of ocular following velocities and the adaptive mechanism that induces perceptual motion after-effects. This similarity is discussed.

Acceleration↗
PubMed1978

Stimulus-governance and the hyperkinetic syndrome.

The hypothesis that hyperkinetic children are stimulus-governed was tested. In a sample of 39 nonmedicated hyperkinetic boys 26 were found to be stimulus-governed. In a control sample of 20 nonmedicated boys 6 were found to be stimulus-governed. An association was found between the hyperkinetic syndrome and stimulus-governance. The hypothesis is raised that response to methylphenidate is related to stimulus-governance. Several issues raised by the research are discussed.

Adolescent↗
PubMed1992

The McCollough effect as a measure of central cholinergic activity in man.

The McCollough Effect (ME) is an orientation contingent colour after-effect which has been proposed as an indicator of central neurotransmitter activity. Shute (1979) suggested that the ME could reflect a hippocampal "forgetting" mechanism which should be inhibited by GABAergic neurones and stimulated by cholinergic neurones. The purpose of the present study was to demonstrate that the ME is in fact sensitive to cholinergic and anticholinergic drugs and to compare its sensitivity to more conventional tests of psychomotor and cognitive function. Ten healthy subjects received single doses of physostigmine (0.75 mg SC), hyoscine (1.2 mg), temazepam (20 mg), flecainide (200 mg) or placebo in a double-blind double-dummy presentation. Subjects were tested on a battery of psychomotor and cognitive function tests at baseline and 1 h, and adapted to the ME at 1.5 h. Visual analogue rating scales and conventional tests of psychomotor function and saccadic eye movements indicated that both subjective and objective measures of arousal were impaired by temazepam. The subjective, but not the objective, measures of arousal were also impaired by both hyoscine and physostigmine, but not by flecainide. Initial strength and duration of the ME were decreased by physostigmine and increased by hyoscine and temazepam, relative to placebo (P less than 0.01). Thus, the ME is capable of detecting cholinergic, anticholinergic and GABA mimetic drug effects in man, in therapeutic doses.

Adaptation, Ocular↗
PubMed2002

Prism adaptation with delayed visual error signals in the monkey.

Errors in reaching produced by displacing the visual field with wedge prisms decrease with trials, even when the error is not revealed until the completion of the movement. To examine how much additional delay in visual feed-back the monkey can compensate for, the effects of delaying the visual error signals were studied by presenting the terminal visual images after one of five delays, ranging from 0 to 500 ms. Adaptation was fastest when the delay was 0 or 10 ms, decreased significantly with a delay as small as 50 ms and approached zero when the delay was 500 ms. The size of the after-effect decreased with the delay accordingly. The results indicate that prism adaptation in the monkey critically depends on the availability of visual information within 50 ms of completion of the movement. Comparing the results with those for humans, we suggest that monkey and human share a mechanism of adaptation with a short time window of 50 ms, but the monkey lacks another mechanism of adaptation that allows a visual delay of 500 ms or more in humans.

Adaptation, Ocular↗