Acta ophthalmologica. Supplementum最新文献

Two F40CW fluorescent lamps mounted in an EYS-2404 fixture and 300 nm, 5 nm waveband UV radiation were used to expose pigmented rabbit eyes. The results of the exposures to the eye were evaluated with the biomicroscope, ophthalmoscope, light microscope and electron microscope. The following conclusions were reached: The adverse ocular responses to fluorescent radiation exposure were due to long-duration, broadband radiation. These reactions were more generalized for fluorescent exposures when the cornea and lens are compared to UV exposures. The differences between the levels of threshold exposure needed to cause damage for the fluorescent source and UV radiation were attributed to exposure duration and the rate of delivery of the radiation. Corneal and lenticular damage was mild when compared with UV 300 nm exposures, and the threshold occurred after 8 h to 12 h of exposure. The effect of the radiation was to interfere with the normal functions of the cell while changes to the inert materials in the tissues was secondary to injury to the cell. The damage was mild in the corneal epithelium, somewhat more severe in the corneal endothelium, but minimal in the corneal stroma. Early retinal changes were found after 8 h of exposure to the fluorescent source. These induced changes were evident in the neural retina as spaces and were assumed to represent oedema. The retinal oedema was initially found only in the receptor cell, outer nuclear and nerve fibre layers. Many vacuoles or spaces were located in the junctional area between the ganglion cell and nerve fibre layers while smaller spacing occurred also within the nerve fibre layer. Twelve h of exposure to the fluorescent source produced a further increase in the oedema in the retina. The outer segments of the receptor cells appear to disintegrate and significant open spaces are evident among the inner and outer segments of the receptors. The inner plexiform layer shows an increased number of spaces within and among the neural elements, and the mitochondria appeared to be undergoing changes. The 20-h and longer exposure induced severe changes affecting all layers of the retina. These changes include massive retinal oedema with degenerative signs in all retinal neurons. A sympathetic reaction of the unexposed, contralateral eye occurred as the result of the damage to the exposed eye. Minimal sympathetic responses to the cornea and the lens began at exposure durations at or above 12 h, while the retina showed the sympathetic reaction beginning at 8 h.(ABSTRACT TRUNCATED AT 400 WORDS)

Visually guided behaviour was studied in cats after various lesions of the central nervous system in order to obtain further information about the functional capacity and developmental plasticity of subcortical visual areas. Hemidecortications were made in all cats either within 5 days of birth (neonatal) or more than one year after birth (adult). In addition the optic chiasm was transected at another time in some cats, or the optic tract contralateral to the hemidecortication in the other cats. Visual behaviour was investigated with several tests: Locomotion among obstacles (free field). Search for openings of chambers (labyrinth). Jumping from/between boxes of different heights (jumpbox). Object vision and visual field (fish-picking cage). Visual learning (T-maze). Pupillary light reactions. Visual placing reactions. Reactions to moving visual stimuli. The hemidecortications caused different visual defects for the adults and the neonatals, which in addition showed varying prominence depending on type of test. All cats showed defects which were caused by hemianopia. Less defects were found in the free field, labyrinth and jumpbox tests for the neonatals compared to the adults. The difference is attributed to a better ability of the neonatals to utilize subcortical visual areas for visual orientation in space. The subsequent optic chiasm or optic tract sections permitted comparison between the functional capacity of crossed and uncrossed retinal fibres to subcortical structures. The uncrossed fibres were found to be unable to maintain any visually guided behaviour even for the above described neonatals. It appears likely that the better vision of the neonatally hemidecorticated cats was mediated via crossed retinal fibres to subcortical structures. It was eventually possible to demonstrate visually guided behaviour which was mediated via subcortical structures also in the adult hemidecorticated cats in the T-maze. The residual vision consisted of an ability to discriminate contrast differences. The present findings emphasize the potential functional importance of subcortical visual areas in the cat, especially after early brain damage. The differential findings from the different tests have shown the limitations of single test investigations. The presence of learnt visual behaviour in the absence of spontaneous visual behaviour for individual animals of this study advocates for greater use of spontanous behaviour for investigations of visual defects caused by brain lesions.