Differential regulation of brain beta-adrenoceptor subpopulations in aging rodents.
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Aging↗
Biomedical subjects
C Viticchi
Publications and source records attributed to C Viticchi.
Age-related alterations of isoproterenol-stimulated adenylyl-cyclase activity are partially corrected by thymic graft.
Previous experimental results have demonstrated progressive impairments in beta-adrenergic responsiveness with advancing age. Beta-adrenoceptors are involved in the alterations as their density progressively decreases during aging. Alterations in both in vivo responsiveness and receptor density are corrected by neonatal thymic grafts. In the present paper adenylyl-cyclase (AC) activity has been studied in the same animal models used before. Results show that no statistically significant changes can be observed when AC is assayed in absence of beta-adrenergic stimulation. On the contrary, when assayed after Isoproterenol stimulation, AC activity shows a shift of the peak and a decrease of its height in aged animals. A neonatal thymus grafted into old recipients one month before the experiment was performed, is capable of correcting the altered height of the peak but not the peak concentration.
Adenylyl Cyclases↗
Thymus-induced recovery of age-related decrease of brain cortex alpha- and beta-adrenoceptors.
It has previously been demonstrated that thymus exerts a regulatory influence on beta-adrenergic system during aging. In particular, it has been shown that thymus can correct the beta-adrenoceptor density decrease in old mice. In the present paper results of experiments are reported dealing with the influence of the thymus on alpha-adrenoceptors of mouse brain cortex. Both subtypes of alpha-adrenoceptors are studied separately, using different labelled ligands. Results show that alpha 1-adrenoceptor density decreases in old animals, while alpha 2-adrenoceptor density does not change significantly. A neonatal thymus grafted into old recipients is capable of correcting the alteration observed in old mice. The differential impairment of alpha-adrenoceptors resembles that one previously observed on beta-adrenoceptors, where beta 1-type decreases in number during aging with a parallel decrease of adenylyl-cyclase activity, while beta 2-type remains unchanged.
Adenylyl Cyclases↗
Influence of age on the thyroid hormone-induced up-regulation of beta-adrenoceptors in mouse brain cortex.
The influence of ageing on the ability of the brain cortex beta-adrenoceptors to be regulated by very short stimulation with thyroid hormones has been investigated. Experiments were performed in 3-, 10-, 17- and 22-month-old mice using both thyroxine (T4) and triiodothyronine (T3) as stimulators and analyzing beta-adrenergic receptor characteristics 15 and 60 min after hormone injection. Results showed that a statistically significant up-regulation is present in both young and old mice when treated with T3. On the contrary, after T4 injection only 3-month-old animals respond to such a short-term treatment, whereas older adult and old animals showed not statistically significant changes. Thus, the impairment in the T4-induced up-regulation starts already in adult mice and does not seem to further increase progressively with advancing age. From these findings it is suggested that the lack of responsiveness of beta-adrenoceptors to T4 but not to T3 stimulation in adult and old mice may be due to relatively early impairment in the transformation of T4 into T3.
Age Factors↗
Thymic involution and aging processes.
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Aging↗
Ageing and thymus-induced differential regulation of beta 1 and beta 2 adrenoceptors of mouse brain cortex.
Two questions have been addressed by the present paper, that is, the differential influence of age on beta 1 and beta 2 receptors and the thymus-induced recovery of such changes in receptor density and affinity have been assayed in brain cortex of Balb/c-nu mice of different ages. Results have shown a progressive decrease of beta 1 receptor density with advancing age, while no statistically significant changes were observed in beta 2 receptor density. Receptor affinity did not show any changes among the various groups examined. The influence of the thymus on receptor characteristics has been studied comparing young, old and thymus-grafted old mice. Total receptor density, which is decreased in old animals, can be up-regulated by thymus graft in old recipients. Interestingly, such a corrective effect is exerted only on the beta 1 population, the beta 2 receptor not being significantly affected. Thymic graft, therefore, acts just on the population which is found altered during ageing.
Aging↗
Impaired adaptive receptor regulation: an index of aging?
Many neuroendocrine functions are altered in old animals and their study may represent important steps in the understanding of the mechanisms of aging. A deeper insight, however, can be achieved by investigating the responsiveness to stimuli, which may reveal alterations not evident in the unstimulated conditions. At this level of study, many of such impairments have been found to be caused by receptor changes. In the present paper a third level of study is suggested in order to gain evidence of some remote failure of adaptive processes strictly linked to intimate mechanisms of aging. As at the second level of study different receptor characteristics can frequently be found at the basis of age-related alterations of biological responsiveness, at the proposed third level altered capacity of receptor regulation may be hypothesized as responsible for altered cell adaptation following hormone and drug stimuli. Experimental data are given which support this view. The possibility that receptor regulation may be used as an index of aging is suggested. This hypothesis leads to the problem of judging the validity of biological parameters deputed to represent good indices of aging. In order to solve this problem, the potential use of a mathematical model of mortality kinetics is discussed.
Adaptation, Physiological↗
Thymic regulation of brain cortex beta-adrenoceptors during development and aging.
The influence of the thymus on beta-adrenoceptors has been studied in the brain cortex of mice during developing and aging. Affinity of beta-adrenoceptors shows no statistically significant changes in the various animal models investigated. Receptor density shows a fall in both athymic nude mice and in old normal mice. Receptor density, in particular, decreases progressively with advancing age. It has been demonstrated that thymus exerts a regulatory role in both development and aging, as a neonatal thymic graft is capable of reversing the receptor impairments found in young athymic nude mice and in old normal mice.
Aging↗
Cytoplasmic contaminants in Triton X-100 washed rat liver nuclei - a possible way of further purification.
The presence of cytoplasmic contaminants is demonstrated in preparations of rat liver nuclei, even after washing with Triton X-100. They can be removed by incubation at 37 degrees C in a medium of low-salt concentration.
Animals↗
Age-dependent change of the protein-bound phosphorus in rat liver cell nuclei.
Some aspects of the metabolism of the protein-bound phosphorus were examined on isolated rat liver cell nuclei in function of age. The protein complement of the nuclei was separated into 5 non-histone and one histone fractions by means of salt and acid extraction. The phosphorus content of the fractions was determined and the rate of phosphorylation and dephosphorylation was measured after 32P labelling. The supernatant of the in vitro phosphorylation system contained a lower amount phosphorus but showed high phosphorylation rate. For several parameters such as the relative amounts of the non-histone proteins, the net phosphorus contents, the newly incorporated phosphorus/unit protein and the phosphatase activity in the nuclei a common pattern was found in function of age; intermediate, maximum and low or intermediate values for the age-groups of 4--6 months, 16--18 months and 24--28 months respectively. The possible implication of the nuclear non-histone proteins in the process of ageing is discussed.
Aging↗