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Biomedical subjects

S W Scheff

Publications and source records attributed to S W Scheff.

10 recordsLinked to original sources
PubMed1992

Amygdala cell loss and atrophy in Alzheimer's disease.

The amygdala and its subnuclei undergo severe volumetric atrophy in Alzheimer's disease (AD). To determine whether this atrophy is due to loss of neuropil, specific neuronal populations, or both, we evaluated the number, size, and packing density of neurons and glia in the cortical and magnocellular basal amygdaloid subregions. The neuropil fraction did not change with AD in either region. Despite a mean 35% increase in cell packing density in the AD amygdala, total numbers of neurons and glia within tissue sections were reduced significantly; medium and large neurons were preferentially affected. The total number of small neurons was stable in the AD sample despite sharp reductions in nuclear size, suggesting that AD also results in pronounced amygdaloid neuronal shrinkage. Differences in the degree of cell loss between the two nuclei as well as changes in glial cell numbers are discussed in relation to characteristic AD neuropathology and relevant anatomical connectivity.

Aged↗
PubMed1992

Neurotrophic effects of steroids on lesion-induced growth in the hippocampus. II. Hormone replacement.

The mediation of lesion-induced sprouting in the nervous system is a complex interaction of local membrane factors and circulating hormones. This series of studies examines the reactivity of the sprouting response of both male and female subjects under different hormonal conditions. Young adult male and female Sprague-Dawley rats which were gonadectomized (GDX) and adrenalectomized (ADX) underwent a unilateral entorhinal cortex lesion, which partially denervates the molecular layer of the ipsilateral hippocampal denate gyrus. At the time of the lesion, each animal received hormonal therapy. Fifteen days post-ERC-ablation the brains were analyzed for changes in reactive fiber outgrowth in the hippocampal commissural/associational afferents. Fiber outgrowth in females in the "asteroidal" (GDX/ADX) condition was unaffected. Asteroidal males demonstrated a decreased response. Gonadal steroid replacement, estrogen or testosterone, enhanced outgrowth in both asteroidal males and females. Glucocorticoid replacement suppressed outgrowth in both asteroidal males and females. Gonadal steroids clearly have neurotrophic activity which is interactive with glucocorticoid activity. Glucocorticoids under the GDX/ADX conditions in vivo have a negative impact on fiber outgrowth in both sexes. The effect of glucocorticoids is most dramatic when compared to the outgrowth of asteroidal animals without additional hormonal supplementation.

Adrenal Cortex Hormones↗
PubMed1979

The specificity of reactive synaptogenesis: a comparative study in the adult rat hippocampal formation.

The CA1 region of the hippocampus in the mature rat is shown to possess the capacity to form new synapses following a lesion of either the commissural afferents, which removes 41% of the synaptic input to stratum radiatum, or commissural and associational afferents, which destroys 74% of the synaptic input. With both types of lesion, extensive reinnervation occurs without obvious changes in lamination of afferent fibers and without accompanying changes in the acetylcholinesterase-(AChE) staining pattern. This is in contrast to what is known to occur in the hippocampal dentate gyrus following an ipsilateral entorhinal lesion where afferent lamination is reordered and where AChE-staining intensifies. A comparison between the disparate patterns of reinnervation in these closely related structures affords the opportunity to examine some of the specific factors that may regulate synaptic readjustments in brain.

Acetylcholinesterase↗
PubMed1979

Glutamate as a CNS transmitter. I. Evaluation of glucose and glutamine as precursors for the synthesis of preferentially released glutamate.

Slices of the molecular layer of the dentate gyrus of the hippocampal formation were incubated with either [14C]glucose, [14C]pyruvate or 14C glutamine and the efflux of endogenous and radioactive glutamate was monitored under various conditions. After prelabeling with either [14C]glutamine or [14C]glucose elevation of K+ concentration to 56 mM (Ca2+ free) increased efflux of endogenous and [14C]glutamate. Introduction of Ca2+ into the elevated K+ medium further increased the efflux of endogenous glutamate and radioactive glutamate derived from any of the precursors tested. In glutamine containing media, the increase in glutamate efflux as well as basal efflux was considerably higher than in the absence of glutamine and the specific activity of glutamate release was higher than that in tissue. Thus glutamine was superior to glucose or pyruvate as precursor and most specifically labeled the putative transmitter pool of glutamate. Similar experiments were carried out 4 and 14 days after a unilateral lesion in the entorhinal cortex which provides about 60% of the total synaptic input to the dentate granule cells. The Ca2+ dependent release of glutamate derived from either glucose or glutamine was markedly reduced on the operated side. This result suggests that the transmitter pool of glutamate is in perforant path terminals and can be synthesized from glucose or glutamine.

Animals↗
PubMed1979

Compensatory synapse growth in aged animals after neuronal death.

The capacity of neurons to grow new synapses following partial denervation has been studied in the brain of aged rats and compared to that of younger animals. Lesion induced synapse formation is reduced in aged rats in the hippocampus and septum, two brain areas which show particularly robust growth responses in younger animals. The rate of growth as well as the final magnitude of the response is diminished in aged animals. A possible mechanism for the decreased growth response in aged animals is discussed in light of current models of reactive synaptogenesis. The loss of a compensatory growth response in the aged animal may be one of the factors which contribute to decreased brain plasticity and the slower and poorer recovery from brain damage following injury.

Aging↗
PubMed1978

Decrease in adrenergic axon sprouting in the senescent rat.

When the septal area in young adult rats is denervated by a lesion of the fimbria-fornix, adrenergic fibers proliferate within the denervated area. The same operation performed on aged animals gives rise to a qualitatively similar but quantitatively less pronounced response. This reduction in reactive growth may reflect a decreased capacity of the aged brain to remodel its circuitry and restore lost function.

Adrenergic Fibers↗