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R J Deeley

Publications and source records attributed to R J Deeley.

3 recordsLinked to original sources

A simple parametric model of the human ocular modulation transfer function.

The ocular modulation transfer function (MTF) has an important role in many investigations into human vision. It can be approximated by the equation MT = exp [-(SF/SFc)n], where MT, SF, SFc and n are the modulation transfer, spatial frequency, frequency constant and MTF index respectively. In a theoretical study, the parameters n and SFc were determined by a mathematical method from previously published data. A general equation was deduced expressing the MTF as a function of pupil size for diameters of 1.5-7.5 mm. For pupil diameters below 1.5 mm different equations providing MTFs as a function of pupil diameter have been produced. These are based on the assumption that for these pupil diameters diffraction and retinal scatter determine the optical degradation. The use of these models is described in studies on spatial vision, where they have widespread applications and the effects of optical degradation are frequently neglected.

Contrast Sensitivity

The effect of optical degradation on the contrast sensitivity function measured at the fovea and in the periphery.

Contrast sensitivity functions (CSF's) were measured for a zone of 0.5 degree angular radius at the fovea and for annular zones extending from 0.5 degrees eccentricity to 1 degree, from 1 to 2 degrees and from 2 to 4 degrees. The effect of optical degradation was taken into account by the application of a correction factor determined from the Modulation Transfer Function (MTF). Using the reciprocal of the peak of the CSF [1/SF (max)] as a parameter, the effect of applying the MTF correction on the CSF with eccentricity was determined. The effect of applying an MTF correction is significantly to increase the rate of change of 1/SF (max) with eccentricity. Since it has been reported that hyperacuity is relatively unaffected by optical degradation, it is proposed that the differing effects of optical degradation between grating acuity and hyperacuity may account, at least partially, for the different rates of decline of these thresholds with eccentricity. The implications of this proposal for M-scaling theories and strategies are considered.

Fovea Centralis

Changes in body weight and food-related behaviour induced by destruction of the ventral or dorsal noradrenergic bundle in the rat.

Three experiments contrasted the effects of 6-hydroxydopamine-induced lesions of the ventral noradrenergic and dorsal noradrenergic projections, predominantly to hypothalamus and cortex, respectively, upon body weight changes and food-related behaviour in the rat. In general, ventral noradrenergic bundle lesions enhanced weight gain and these effects were exaggerated by the provision of palatable cheese to the standard chow diet. In contrast, lesions of the dorsal noradrenergic bundle produced minor changes in body weight. Associated with the effects of ventral noradrenergic bundle lesions were hyperphagia, enhanced suppression of intake of food adulterated with quinine, (at high concentration), a small attenuation of food neophobia, and enhanced acquisition, but not performance, of the eating response to tail-pinch stimulation. These ventral noradrenergic bundle lesions failed to alter basal activity levels, amphetamine anorexia or the diurnal pattern of eating or activity. In contrast, lesions of the dorsal noradrenergic bundle did not produce either hyperphagia or enhanced rejection of food adulterated with quinine. However, there was a strong attenuation of food neophobia and a retarded acquisition (but unimpaired performance) of eating in response to tail-pinch stimulation. The results are discussed in connection with previous studies of ventral and dorsal noradrenergic bundle lesions, with the effects of ventromedial hypothalamic lesions and with the underlying behavioural and physiological processes that mediate these contrasting effects of different neuroanatomical patterns of central noradrenaline depletion.

Animals