Chronic lead administration in neonatal rats: electron microscopy of the retina.

The morphologic effects on the retina resulting from chronic lead exposure were assessed in neonatal rats. Newborn rats nursed from dams were given a low (0.115%) or a high (4.5%) concentration of lead in their diet. At day 21 the pups were weaned to the mother's diet. The retinas of the pups were studied by electron microscopy at various ages up to day 60. High and low lead concentrations produced necrosis of photoreceptor cells and cells of the inner nuclear layer. The high lead concentration, in addition, was associated with swelling of endothelial cells of the retinal vessels and narrowing of the lumen. Increased permeability of the retinal vessels and pigment epithelium to horseradish peroxidase was also observed under the high-dose condition. The authors conclude that lead can produce direct neuronal damage and, at high doses, produces retinal vascular lesions and alteration of the blood-retinal barrier.

Heredofamilial retinal dystrophy in Guinea baboons. II. Electron microscopic observations.

Electron microscopic study of an inherited retinal degeneration in Guinea baboons disclosed primary pathologic alterations in photoreceptor cells. These changes were first seen in the perifoveal region. Cell death occurred in two forms: hydropic degeneration and densification and/or necrosis. The hydropic type was mainly associated with cone cells, whereas densification and/or necrosis was largely seen in rod cells. Lamellar bodies and granular membrane-bound inclusions were noted in the inner segments and soma. Mitochondria were vacuolated and formed membranous whorls. Bundles of filaments were arranged in parallel array in the soma synaptic endings. Clusters of tubules were present in the synaptic terminals. Preliminary biochemical studies on these animals have yielded no clues to the pathogenesis of the retinopathy.

Heredofamilial retinal dystrophy in Guinea baboons. I. A histopathologic study.

We performed a histopathologic study of a heredofamilial retinal dystrophy in a colony of Guinea baboons. A bull's-eye appearance was noted in the maculas of six baboons of three generations. Histologic examination of 13 eyes from this colony showed primary degeneration of both rod and cone cells initially in the parafoveal region, which subsequently involved the photoreceptor cells of the equator and periphery of the retina. The retinal pigment epithelium and choriocapillaris showed mild changes in the early stages. This disease in baboons was compared with various human retinomaculopathies.

Selective neurochemical and histological lesions in rat hippocampus following chronic trimethyltin exposure.

Trimethyltin exerts a unique and selective pattern of toxicity which may be related to the neurochemical innervation of the hippocampus. Rats were chronically administered trimethyltin and the kinetics of neurotransmitter uptake was assessed in hippocampal synaptosomes. Additional rats were prepared for histological examination. Uptake of the endogenous hippocampal amino acid neurotransmitters glutamic acid and gamma-aminobutyric acid showed dose-dependent alterations. Uptake of norepinephrine was not significantly affected. Histopathological analysis indicated differential neuronal loss within classically defined hippocampal cell fields.

An inherited retinopathy in collies. A light and electron microscopic study.

A recessively inherited retinopathy in collies aged 8 to 189 days was studied by light and electron microscopy. The disease is produced when the outer segments of rods and cones fail to develop normally. Retinal pigment epithelial changes found in several litters appeared to form a separate disease entity. We compared the collie retinopathy with other canine models and the collie ectasia syndrome.

Stimulation of rat medial or sulcal prefrontal cortex during passive avoidance learning selectively influences retention performance.

Low-level unilateral electrical stimulation was delivered during passive avoidance learning through a bipolar electrode to the prefrontal cortex of the adult albino rat. No brain stimulation was applied during a retention test measured 24 h later. Ventromedial prefrontal cortex stimulation produced retention impairment over and above that observed with chronic electrode implantation. Sulcal cortex stimulation, in contrast, actually attenuated the retention deficit produced by chronic implantation in the sulcal cortex. Stimulation of an afferent common to both prefrontal regions, the dorsomedial thalamus, resulted in retention disruption, but stimulation of another common afferent, the locus coeruleus, did not. Acquisition of the inhibitory response was not affected by stimulation of any of the above brain regions. The present results demonstrate, again, that the functional role in memory of particular brain regions can be dissected by low-level electrical stimulation. The functional separation of rat sulcal and medial cortices revealed by the effects of stimulation suggests that these prefrontal subfields subserve different functions in the information storage process.