Biomedical subjects

A J Scheetz

Publications and source records attributed to A J Scheetz.

5 recordsLinked to original sources

PubMed1990

Light, vision, and aging.

Recent research on aging of chromatic and spatial vision processes is reviewed. Changes in these visual processes with advancing age are largely continuous. Age-related declines in visual performance may be explained in terms of reductions in the illuminance of the visual stimulus due to changes in the ocular media and losses of efficiency at a neural level. Thus, some prominent characteristics of the senescent visual system are similar to those of the younger visual system operating at a lower ambient light level. One important determinant of retinal aging may be the light history of the individual, i.e., cumulative exposure to high-energy photons from solar radiation may accelerate retinal aging. If these abstractions from the literature are valid, then it will become more important to control the light environment throughout the life span.

Aged↗

PubMed1988

Astrocyte proliferation precedes a decrease in basket cells in the dentate fascia following chronic ethanol treatment in mice.

The effect of chronic ethanol administration on the density of basket cells in the dentate gyrus of mice selectively bred for their sensitivity to acute ethanol exposure (long-sleep, LS and short-sleep, SS) was assessed in two experiments. In addition, the effect of chronic ethanol on the density of dentate granule cells and astrocytes was examined. In the first experiment, mice received 3 weeks of a liquid ethanol diet with 35% of their calories derived from ethanol (EDC). In this experiment, LS mice did not demonstrate a change in the density of granule cells or in the density of basket cells. There was, however, a significant increase in the density of astrocytes as a result of this treatment for the LS mice. The SS mice were unaffected on all measures. In the second experiment, portions of which have been reported previously, mice received a diet with 23% EDC for 3 months. As a result of this exposure, LS mice showed a significant decrease in the density of basket cells, but there was no change in the density of granule cells or astrocytes. There was no difference between controls and experimental mice from the SS group on any of these parameters. These results suggest that at least in the dentate gyrus, chronic ethanol treatment selectively reduces the density of basket cells but only in mice that are more sensitive to the hypnotic effects of acute ethanol exposure. Furthermore, this effect seems to be preceded by an apparent increase in the density of astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗

PubMed1987

The effect of chronic ethanol consumption on the fine structure of the CA1 stratum oriens in short-sleep and long-sleep mice: short-term and long-term exposure.

The effect of chronic ethanol administration on the fine structure of the hippocampal CA1 stratum oriens was examined in two lines of mice selectively bred for their differential sensitivity to acute ethanol exposure (long-sleep, LS and short-sleep, SS mice). Two experiments were performed. In the first experiment, mice received a liquid diet for 3 weeks with the final amount of ethanol being 35% ethanol-derived calories. In the second experiment, mice received 23.5% ethanol-derived calories for 3 months. Quantitative electron microscopy of the dendritic spines and synaptic appositions in the stratum oriens of CA1 revealed an interaction between diet and line of mice, but only in the 3-month exposure condition. This difference was due to a significant decrease in the density of spines and synaptic appositions in the LS mice receiving ethanol. Additionally, baseline differences between lines indicate that the lines are differing in the density of spine synapses in the absence of ethanol treatment. The possible interaction between acute sensitivity to ethanol and differences in fine structure are examined.

Animals↗

PubMed1987

Changes in the frequency of basket cells in the dentate fascia following chronic ethanol administration in mice.

The frequency of basket cells in the granule cell layer of the dentate fascia of Short Sleep (SS) and Long Sleep (LS) mice was determined following 3 months of ethanol exposure. These mice were bred for their differential susceptibility to the narcotic effects of acute doses of ethanol. The ethanol-insensitive SS mice were unaffected by the treatment while the ethanol-sensitive LS mice that received ethanol showed a significant decrease in basket cell frequency over their control group counterparts. These basket cells are thought to control the tonic level of activity of the granule cells. Thus, a decrease in basket cell frequency might lead to higher granule cell activity following chronic ethanol exposure. This effect could counteract the assumed stronger depressant effect of ethanol in the relatively ethanol-sensitive LS mice.

Animals↗

PubMed1987

Effect of chronic ethanol consumption on the fine structure of the dentate gyrus in long-sleep and short-sleep mice.

The effect of short- and long-term chronic ethanol consumption on the fine structure of the dentate gyrus was examined in two lines of mice selected for their differential sensitivity to acute ethanol administration. Quantitative electron microscopic analysis of dendritic spines, axon terminals, and synaptic appositions revealed significant differences between the long-sleep and short-sleep mice. In control preparations, long-sleep mice were found to have larger spine areas and perimeters, larger axon terminals, and longer synaptic appositions than short-sleep mice. In addition, the shape of dendritic spines in the long-sleep mice was significantly more complex than those of short-sleep mice. Ethanol tended to increase this complexity in long-sleep mice only. Ethanol had only a limited effect on the other anatomical measures. The results provide evidence for ultrastructural differences between the nervous systems of these lines of mice which may have a role in their differential sensitivity to acute ethanol administration.

Alcoholism↗