Biomedical subjects

V H Perry

Publications and source records attributed to V H Perry.

4 recordsLinked to original sources

PubMed1979

The ganglion cell layer of the retina of the rat: a Golgi study.

In whole-mounts of Golgi stained rat retinae four cell types are described in the ganglion cell layer. Three of these cell types are considered to be analogous to the alpha, delta and gamma cells described in the cat retina by Boycott & Wässle (1974). The fourth cell type is thoughtt to be a displaced amacrine cell. All the cell types described are present in all parts of the retina. There is no evidence for an increase in dendritic field size with increasing distance from the optic disk.

Animals↗

PubMed1979

The projection of the temporal retina in rats, studied by retrograde transport of horseradish peroxidase.

Horseradish peroxidase (HRP) was injected unilaterally into the lateral geniculate nucleus or tectum, or both, in 26 hooded rats in order to mark the exact extent of the retina from which uncrossed optic axons arise. This region occupied about a quarter of the retina, in the temporal periphery, following thalamic injections, but a much smaller region following tectal injections. By comparing the proportions of HRP positive neurones in nasal and temporal retinae of both eyes it was shown that: (1) within the region supplying uncrossed axons the majority of the ganglion cells nevertheless project contralaterally, (2) a large proportion of the ganglion cells from the temporal crescent project bilaterally, which does not occur from the remainder of the retina, (3) ganglion cells of all sizes contribute to both ipsilateral and contralateral projections. The results also support earlier suggestions that the smallest neurones in the ganglion cell layer do not send an axon into the brain, and are therefore not ganglion cells.

Animals↗

PubMed1979

The effects of unilateral cortical and tectal lesions on retinal ganglion cells in rats.

The ganglion cell layer of the retina was examined for retrograde transneuronal degeneration after removing the striate cortex unilaterally in infant or adult rats. No significant degeneration occurred, even after a survival time of 15 months, and the rat is therefore unlike other mammals in which the phenomenon has been studied. A possible explanation that most optic axons bifurcate in rats and that the tectal branch can sustain the ganglion cell after the branch to the dorsal lateral geniculate nucleus has degenerated following removal of striate cortex was ruled out by the demonstration that combined unilateral removal of striate cortex and superior colliculus in adults was similarly ineffective. Unilateral removal of the superior colliculus alone also failed to affect ganglion cells of adult rats but produced conspicuous degeneration in infants. The greater vulnerability of the infantile developing visual system casts doubt on the common assumption that the effects of brain damage are less severe in infants than adults.

Animals↗

PubMed1979

Changes in the retino-fugal pathways following cortical and tectal lesions in neonatal and adult rats.

Several months after unilateral removal of the striate cortex or superior colliculus, or both, in infant and adult rats the retinal projections were studied autoradiographically. The retinal projection areas in adult-operated animals were not different from those of unoperated controls, but aberrant pathways were found in the infant group. Following removal of striate cortex there was a small aberrant pathway to the lateral posterior nucleus of the thalamus (LP) and possibly to the pretectum. After removal of the superior colliculus there was a conspicuous aberrant projection to LP, which was even more prominent after combined removal of striate cortex and superior colliculus. The results support the proposal that when the normal field of termination is damaged, either directly by a tectal lesion or indirectly by a cortical lesion, axons grow and innervate LP, which has been partly deafferented by the lesion and which consequently possesses vacant synaptic space. Although the different consequences of early and late lesions may indicate that only infantile damaged terminals can redistribute themselves an alternative is that in infants many axons have not yet reached their normal terminal sites at the time of operation and that only those axons have the ability to continue growing and to form an aberrant pathways. The role of the aberrant pathway in vision is unknown.

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