PubMed Health⌕ Search

Biomedical subjects

C E Finch

Publications and source records attributed to C E Finch.

At least 199 records · Page 11Linked to original sources
PubMed1980

Reduced dopaminergic binding during aging in the rodent striatum.

[3H]Spiroperidol and [3H]ADTN ( 2-amino-l,7-dihydroxy-1,2,3,4-tetra hydronaphthalene) binding were used to assay for dopamine receptors in aged C57BL/6J mouse striatal membranes. [3H]spiroperidol binding declined linearly with age starting at 3 months. By 28 months, spiroperidol binding was only about 50% of the 3 month value. Dissociation constants dissociation rates and binding inhibition by (+)-butaclamol (antagonist) and apomorphine (agonist) were similar, suggesting that the age-related loss of spiroperidol binding was due to a loss in receptor number and not an alteration in binding affinity. [3H]ADTN binding also declined with age, but the losses tended to be about twice as large as those seen for spiroperidol. Consideration of possible mechanisms of receptor loss with age indicate that nigrostriatal denervation effects cannot explain all aging changes in striatal dopaminergic functions. The loss of receptors with age may derive from a loss of striatal neurones on which residue a population of dopaminergic binding sites.

Aging↗
PubMed1980

Studies on the biochemistry of the brain during aging.

There is little doubt that aging changes occur in specific brain cells and neural pathways. Since some of these changes occur in short-lived rodents which probably have no major vascular pathology [48], there may be a general phenomenon of aging in the brain neurotransmitter functions in short- and long-lived mammals. It remains to be discovered how the genome regulates the changes in catecholamine neurotransmitter functions and, further, how these changes relate to normal and pathologic age changes.

Aging↗
PubMed1979

Aging and unusual catecholamine-containing structures in the mouse brain.

Brains of C57BL/6J mice, aged 4, 8 and 20--29 months, were examined by the Falck-Hillarp histochemical fluorescence technique. Numerous large, intensely fluorescent green to yellow-green spots (LIFS) were observed in the brains of senescent mice. LIFS were generally round to ovoid in shape and ranged in size from about 10 micrometer to about 30 micrometer. Histochemical and pharmacological procedures and spectral analysis indicated that the formaldehyde-induced fluorescence of the LIFS was due to the presence of catecholamines (CA) rather than aging pigment. Their distribution in the brain suggests an association with nerve axons or terminals rather than cell bodies. The number of LIFS in the hypothalamus increased progressively during aging. It is proposed that LIFS may represent age-related, unusual CA accumulation in enlargements proximal to axonal or terminal portions undergoing spontaneous degeneration.

Aging↗
PubMed1979

Neuroendocrine mechanisms and aging.

Evidence describing altered neuroendocrine function during aging from this and other laboratories is reviewed, with focus on changes in the brain-pituitary-ovarian-adrenal-hepatic and in the brain-pituitary-ovarian systems. Difficulties in interpreting the discordant data on age-related changes in pituitary function are discussed. Among mechanisms of reproductive aging are changes at both the ovarian and hypothalamic level (including reduced catecholamine levels, turnover, and synaptosomal uptake). However, it cannot yet be concluded that impairments of hypothalamic catecholamine metabolism are the primary cause for the loss of regular cycles. Evidence for dopaminergic impairments in the basal ganglions of humans and rodents during normal aging suggests that these changes may be a general phenomenon of aging. Although the origins of the changes are not yet known, neuronal cell loss in the substantia nigra would not seem to be the only cause.

Adult↗