Effect of Aging on the Activities of Acetylcholinesterase, Na+, K+-ATPase and Mg2+-ATPase in Rat Pituitary and Hypothalamus

1998 ◽  
Vol 53 (3-4) ◽  
pp. 168-172 ◽  
Author(s):  
Stylianos Tsakiris ◽  
Panagoula Angelogianni ◽  
John C. Stavridis
Keyword(s):  
Atpase Activity ◽  
Ache Activity ◽  
Energy Production ◽  
Metabolic Energy ◽  
Adult Rats ◽  
Neural Excitability ◽  
Age Related ◽  
Rat Pituitary ◽  
Old Rats

Abstract Acetylcholinesterase (AChE), Na+, K+-ATPase and Mg2+-ATPase activities were esti­mated in homogenised rat pituitary and hypothalamus of 4-and 22-month-old rats. AChE activity was not altered in the pituitary of aged com pared to adult rats, while it was found decreased by about 40% in the hypothalamus. Na+,K+-ATPase activity remained stable in the hypothalamus, while it was decreased by about 38% in the pituitary. Mg2+-ATPase activ­ity remained unchanged in the hypothalamus, but was increased by about 83% in the pitu­itary. This pituitary Na+, K+-ATPase inactivation may result in pathological mood and de­creased neural excitability and metabolic energy production in aged animals.The age-related alterations of AChE , Na+, K+-ATPase and Mg2+-ATPase activities may reflect changes in secretion and responses of some hormones of pituitary and hypothalamus.

Age-related changes of growth hormone secretory mechanisms in the rat pituitary gland

1991 ◽  
Vol 131 (2) ◽  
pp. 251-257 ◽  
Author(s):  
M. Parenti ◽  
D. Cocchi ◽  
G. Ceresoli ◽  
C. Marcozzi ◽  
E. E. Müller
Keyword(s):  
Growth Hormone ◽  
Male Rats ◽  
Lower Percentage ◽  
Aged Rats ◽  
Adult Rats ◽  
Infant Rats ◽  
Age Related ◽  
Rat Pituitary ◽  
Old Rats ◽  
Stimulation Of

ABSTRACT The mechanisms underlying the age-related decrease and increase in somatotroph responsiveness to growth hormone-releasing factor (GHRF) and somatostatin respectively were studied in rat pituitary membranes in vitro. Basal adenylate cyclase (AC) activity was similar in pituitary membranes from rats of 8 days (either sex) and male rats of 3 months, but it was almost threefold higher in membranes from male rats of 21–23 months. GHRF induced a lower percentage stimulation of AC activity in membranes from infant and old than adult rats. Somatostatin inhibited stimulation of AC induced by forskolin more effectively in membranes from adult than infant and old rats. In parallel experiments, since the tissue we used is formed by a mixed population of pituitary cells, we evaluated, for comparison, the effect on AC of neurohormones, i.e. vasoactive intestinal polypeptide (VIP) and dopamine which act primarily on lactotrophs. VIP induced a lower fold-stimulation of AC activity in membranes from infant and old than adult rats. Dopamine inhibited forskolin-induced stimulation of AC in the following rank order of magnitude: old, adult and infant rats, and was also more effective in inhibiting basal AC activity in old than in adult rats. The stimulatory and inhibitory G proteins (Gs and Gi) coupled to AC were measured indirectly by evaluating stimulatory and inhibitory effects of different concentrations of GTP on AC. GTP, at stimulatory concentrations, increased AC activity in membranes from infant and adult rats similarly whereas its effect was significantly greater in membranes from old rats. Conversely, GTP, at inhibitory concentrations, decreased AC activity similarly in membranes from adult and infant rats, whereas in old rats inhibition was apparent at more than a tenfold lower concentration of GTP. These data suggest (1) that the greater somatotroph sensitivity to GHRF in terms of GH secretion of the early postnatal period is not due to supersensitive GHRF receptors but rather may be accounted for, at least partially, by the low function of somatostatinergic receptors; (2) that the inability of GHRF to stimulate GH release in aged rats probably results from an uncoupling between the GHRF receptor and the G protein; and (3) that in aged rats the decreased ability of somatostatin to inhibit AC activity, in spite of the high Gi activity, results from a reduced number of somatotroph cells and, hence, receptors. Journal of Endocrinology (1991) 131, 251–257

Pituitary-adrenal response to bacterial endotoxin in developing rats

1988 ◽  
Vol 255 (4) ◽  
pp. E525-E530 ◽  
Author(s):  
L. Witek-Janusek
Keyword(s):  
Plasma Corticosterone ◽  
Neonatal Rat ◽  
Bacterial Endotoxin ◽  
Plasma Acth ◽  
Adult Rats ◽  
Age Related ◽  
Corticosterone Response ◽  
Adrenal Response ◽  
Old Rats ◽  
Related Pattern

The neonatal rat is very sensitive to the lethal effects of bacterial endotoxin. Because of the adaptive importance of pituitary-adrenal secretions to stress, this study examined the ontogeny of the plasma corticosterone and adrenocorticotropic hormone (ACTH) responses to endotoxin. The lethal sensitivity of young rats to endotoxin ranged from 0.5 to 30 mg/kg (ip) in the 1- to 21-day-old rat. After endotoxin treatment, the 1- and 2-day-old rat showed marked elevations of corticosterone similar in magnitude to that seen in 21-day-old and adult rats; however, significantly depressed corticosterone increments were observed in the 5-, 10-, and 14-day-old rats. This age-related pattern of adrenocortical secretion was correlated with the developing rat's corticosterone response to exogenous ACTH. In contrast, endotoxin administered to 5-, 10-, and 14-day-old rats resulted in increments of plasma ACTH similar to those observed in the 21-day-old and adult rats. Although plasma ACTH levels increased by 84-127% in the 1- and 2-day-old rats, these increases were significantly less than those of rats at all other ages tested. Thus the newborn rat mounts an effective corticosterone response to endotoxin, loses this ability between ages 5-14 days, and regains this response at 21 days of age. Because the hyporesponsive ages exhibit a marked increase in ACTH secretion, the loss of the adrenocortical response to endotoxin appears to be a result of a depressed responsiveness of the adrenal cortex to ACTH.

scholarly journals Pairing Cholinergic Enhancement with Perceptual Training Promotes Recovery of Age-Related Changes in Rat Primary Auditory Cortex

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Patrice Voss ◽  
Maryse Thomas ◽  
You Chien Chou ◽  
José Miguel Cisneros-Franco ◽  
Lydia Ouellet ◽  
...  
Keyword(s):  
Auditory Cortex ◽  
Structural Changes ◽  
Primary Auditory Cortex ◽  
Auditory Training ◽  
Tone Frequency ◽  
Perceptual Training ◽  
Adult Rats ◽  
Functional Changes ◽  
Age Related ◽  
Old Rats

We used the rat primary auditory cortex (A1) as a model to probe the effects of cholinergic enhancement on perceptual learning and auditory processing mechanisms in both young and old animals. Rats learned to perform a two-tone frequency discrimination task over the course of two weeks, combined with either the administration of a cholinesterase inhibitor or saline. We found that while both age groups learned the task more quickly through cholinergic enhancement, the young did so by improving target detection, whereas the old did so by inhibiting erroneous responses to nontarget stimuli. We also found that cholinergic enhancement led to marked functional and structural changes within A1 in both young and old rats. Importantly, we found that several functional changes observed in the old rats, particularly those relating to the processing and inhibition of nontargets, produced cortical processing features that resembled those of young untrained rats more so than those of older adult rats. Overall, these findings demonstrate that combining auditory training with neuromodulation of the cholinergic system can restore many of the auditory cortical functional deficits observed as a result of normal aging and add to the growing body of evidence demonstrating that many age-related perceptual and neuroplastic changes are reversible.

Alterations in dopamine DA1 receptor and G proteins in renal proximal tubules of old rats

1997 ◽  
Vol 273 (1) ◽  
pp. F53-F59 ◽  
Author(s):  
V. Kansra ◽  
T. Hussain ◽  
M. F. Lokhandwala
Keyword(s):  
Atpase Activity ◽  
G Proteins ◽  
Sch 23390 ◽  
Skf 38393 ◽  
Proximal Tubules ◽  
Adult Rats ◽  
Protein Activation ◽  
Proximal Tubular ◽  
Old Rats ◽  
Renal Proximal Tubular

The present study examines the effect of dopamine DA1-receptor agonists on the renal proximal tubular Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity and quantitates DA1 receptors and the coupled G proteins in Fischer 344 model of adult (6 mo old) and old (23 mo old) rats. Dopamine and the preferential DA1-receptor agonist, SKF-38393, produced a concentration-dependent inhibition of Na(+)-K(+)-ATPase activity in proximal tubules from adult rats, whereas the enzyme activity was unaffected by these agonists in the old rats. The binding of DA1-receptor antagonist [3H]Sch-23390 in the proximal tubular basolateral membranes showed a marked decrease (approximately 47%) in the receptor numbers in old compared with adult rats, whereas dissociation constant (Kd) values in old compared with adult rats were not significantly different. Dopamine and SKF-38393 stimulated 35S-labeled guanosine 5'-O-(3-thiotriphosphate) binding in adult rats, but there was no significant effect on the binding in the old rats. Quantification of G2 alpha and Gq/11 alpha using Western analysis revealed a significant increase in quantities of both the G proteins in old rats. The data suggest that a reduction in DA1 receptor number and subsequently reduced G protein activation may be the causative factors for the impairment in DA1 receptor-mediated inhibition of Na(+)-K(+)-ATPase activity in the proximal tubules of old rats.

Age-related differences in angiotensin I metabolism by isolated perfused rat lungs

1980 ◽  
Vol 238 (5) ◽  
pp. R395-R399 ◽  
Author(s):  
K. B. Wallace ◽  
R. A. Roth ◽  
J. B. Hook ◽  
M. D. Bailie
Keyword(s):  
Pulmonary Vasculature ◽  
Lung Mass ◽  
Angiotensin I ◽  
Adult Rats ◽  
Bicarbonate Buffer ◽  
Vasoactive Substances ◽  
Age Related ◽  
Old Rats ◽  
Ace Activity ◽  
Related Increase

The pulmonary vasculature has been implicated in the clearance of several vasoactive substances from the circulation including angiotensin I (AI). In view of the previously reported age-related differences in angiotensin-converting enzyme (ACE) activity of lung homogenates, it was of interest to examine the ability of intact perfused lungs to metabolize AI. Lungs from newborn and adult rats were perfused with Krebs bicarbonate buffer containing 1.0 ng/ml AI in a single-pass, nonrecirculating system. The rate of perfusion was normalized to lung mass. Removal of AI was determined from the transpulmonary difference in radioimmunoassayable AI. Lungs from 7-day-old rats removed a smaller fraction of AI from the circulation than did adult lungs. The age-related increase in AI clearance was accompanied by an increase in pulmonary ACE content; however, enzyme content alone could not account for the observed differences. The increased metabolism of AI by the pulmonary vasculature during development may contribute to the age-related increase in circulating angiotensin II concentrations.

Role of oxidative stress in defective renal dopamine D1 receptor-G protein coupling and function in old Fischer 344 rats

2006 ◽  
Vol 291 (5) ◽  
pp. F945-F951 ◽  
Author(s):  
Riham Zein Fardoun ◽  
Mohammad Asghar ◽  
Mustafa Lokhandwala
Keyword(s):  
Oxidative Stress ◽  
G Protein ◽  
D1 Receptor ◽  
Serine Phosphorylation ◽  
D1 Receptors ◽  
Adult Rats ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Age Related ◽  
Old Rats

Aging is associated with an increase in oxidative stress. Previously, we have reported that dopamine failed to inhibit proximal tubular Na-K-ATPase and to promote sodium excretion in old rats (Beheray S, Kansra V, Hussain T, and Lokhandwala MF. Kidney Int 58: 712–720, 2000). This was due to uncoupling of dopamine D1 receptors from G proteins resulting from hyperphosphorylation of D1 receptors. The present study was designed to test the role of oxidative stress in the age-related decline in renal dopamine D1 receptor function. We observed that old animals had increased malondialdehyde (MDA) levels, a biomarker of oxidative stress, and decreased D1 receptor number and protein in the proximal tubules (PT) compared with adult rats. In old rats, there was increased G protein-coupled receptor kinase-2 (GRK-2) abundance, increased basal serine phosphorylation of D1 receptors, and defective D1 receptor-G protein coupling in PT membranes. Interestingly, supplementation with an antioxidant, tempol (1 mmol/l in drinking water for 15 days), lowered MDA levels and normalized D1 receptor number and protein in old rats to the level seen in adult rats. Furthermore, tempol decreased GRK-2 abundance and D1 receptor serine phosphorylation and restored D1 receptor-G protein coupling in PT of old rats. The functional consequence of these changes was the restoration of the natriuretic response to D1 receptor activation in tempol-supplemented old rats. Therefore, in old rats, tempol reduces oxidative stress and prevents GRK-2 membranous abundance and hyperphosphorylation of D1 receptors, resulting in restoration of D1 receptor-G protein coupling and the natriuretic response to SKF-38393. Thus tempol, by lowering oxidative stress, normalizes the age-related decline in dopamine receptor function.

Expression of acetylcholine receptor mRNAs in atrophying and nonatrophying skeletal muscles of old rats

1998 ◽  
Vol 85 (5) ◽  
pp. 1903-1908 ◽  
Author(s):  
Ronald R. Gomes ◽  
Frank W. Booth
Keyword(s):  
Skeletal Muscle ◽  
Acetylcholine Receptor ◽  
Biceps Brachii ◽  
Male Rats ◽  
Brown Norway ◽  
Mrna Levels ◽  
Adult Rats ◽  
Γ Subunit ◽  
Age Related ◽  
Old Rats

We examined the age-related association in skeletal muscle between atrophy and expression of mRNAs encoding both the γ-subunit of the nicotinic acetylcholine receptor (AChR), and myogenin, a transcription factor that upregulates expression of the γ-subunit promoter. Gastrocnemius and biceps brachii muscles were collected from young (2-mo-old), adult (18-mo-old), and old (31-mo-old) Fischer 344/Brown Norway F1 generation cross male rats. In the gastrocnemius muscles of old vs. young and adult rats, lower muscle mass was accompanied by significantly elevated AChR γ-subunit and myogenin mRNA levels. In contrast, the biceps brachii muscle exhibited neither atrophy nor as drastic a change in AChR γ-subunit and myogenin mRNA levels with age. Expression of the AChR ε-subunit mRNA did not change with age in either gastrocnemius or biceps brachii muscles. Thus changes in skeletal muscle AChR γ-subunit and myogenin mRNA levels may be more related to atrophy than to chronological age in old rats.

Abundance of Na(+)-K(+)-ATPase mRNA is regulated by glucocorticoid hormones in infant rat kidneys

1991 ◽  
Vol 260 (2) ◽  
pp. F192-F197 ◽  
Author(s):  
G. Celsi ◽  
A. Nishi ◽  
G. Akusjarvi ◽  
A. Aperia
Keyword(s):  
Atpase Activity ◽  
Renal Cortex ◽  
Rapid Onset ◽  
Mrna Abundance ◽  
Adult Rats ◽  
Postnatal Maturation ◽  
Before And After ◽  
Intraperitoneal Dose ◽  
Old Rats ◽  
Ouabain Inhibition

The administration of glucocorticoid hormone (GC) accelerates the postnatal maturation of renal Na(+)-K(+)-ATPase activity. This study examines the role of GC for the regulation of the Na(+)-K(+)-ATPase mRNA abundance in renal cortex during development. In 12- to 14-day-old rats an upsurge in serum GC concentration was accompanied by an increase in Na(+)-K(+)-ATPase activity and by an apparent increase in mRNA abundance. In 10-day-old rats injected with a single intraperitoneal dose of betamethasone (T) or diluent (C) the abundances of alpha 1- and beta-mRNAs were 1.8- to 2-fold higher in T than in C rats after 20 min. The mRNA abundance of both subunits was threefold higher after 1 h (P less than 0.01), and it was six- to sevenfold higher after 6 h (P less than 0.01). In any given sample there was a coordinate change in alpha 1- and beta-mRNAs relative to C rats. GC did not appear to induce the expression of any alternative catalytic subunit. The alpha 2-mRNA was not detectable in any experimental protocol. Furthermore, the ouabain inhibition of the Na(+)-K(+)-ATPase, partially purified from the renal cortex, was the same before and after GC. In adult rats injected with betamethasone neither the alpha 1- nor the beta-mRNA abundance was different at any time after injection from those in adult C rats. The rapid onset of the GC effect on mRNA abundance in infant rats suggests that the hormone directly activates the gene for Na(+)-K(+)-ATPase alpha 1-subunit, as well as beta-subunit in the developing kidney, and that GC thereby plays an important role for the postnatal maturation of the kidney.

scholarly journals Modulatory effects of PKC activity on increased 92-kDa gelatinase secretion by neonatal alveolar macrophages

1997 ◽  
Vol 273 (5) ◽  
pp. L989-L996 ◽  
Author(s):  
Christophe Delacourt ◽  
Patricia Rouet-Benzineb ◽  
Christophe Delclaux ◽  
Jeannique L’Hour ◽  
Alain Harf ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Postnatal Period ◽  
Calpain Inhibitor ◽  
Calpain Activity ◽  
Adult Rats ◽  
Age Related ◽  
Key Factor ◽  
Old Rats ◽  
High Level

We previously demonstrated that alveolar macrophages (AMs) from neonatal rats can secrete more 92-kDa gelatinase than AMs from adult rats. In this study, we investigated the role of the protein kinase C (PKC) pathway in the transductional regulation of 92-kDa gelatinase secretion by rat AMs, and we also evaluated maturational changes in this role with increasing postnatal age. After AM stimulation by phorbol 12-myristate 13-acetate (PMA), we observed a dose-dependent increase in gelatinase secretion that was significantly more marked in AMs from 6-day-old rats than in AMs from adult rats and that was inhibited by the PKC inhibitor calphostin C. Adenosine 3′,5′-cyclic monophosphate mimetics or concanavalin A failed to induce an increase in gelatinase secretion by AMs. Time-dependent variations in PKC activity after PMA stimulation differed significantly between 6-day-old rats and adult rats; PKC activity decreased in adult AMs (50%) but remained stable in 6-day-old AMs. We therefore investigated age-related differences in the intracellular proteolytic degradation of PKC, which is thought to be mediated by calpains. Leupeptin, used as a calpain inhibitor, inhibited the decrease in PKC activity after exposure of adult AMs to PMA and induced a greater than threefold increase in PMA-induced gelatinase secretion. Calpain activity was significantly lower in AM extracts from 6-day-old than from adult rats. The physiological implication of these developmental changes in 92-kDa gelatinase regulation was demonstrated by investigation of AMs from 1-day-old rats that showed a high level of spontaneous PKC-dependent gelatinase secretion coexisting with very low calpain activity. We conclude that sustained PKC activity is a key factor in the increased gelatinase secretion by AMs seen during the postnatal period and is due, at least in part, to reduced PKC degradation.

AGE-RELATED CHANGES IN THE METABOLISM OF [3H]TESTOSTERONE IN VITRO BY THE EPIDIDYMIS OF THE IMMATURE RAT

1981 ◽  
Vol 91 (1) ◽  
pp. 43-51 ◽  
Author(s):  
R. G. FOLDESY ◽  
J. H. LEATHEM
Keyword(s):  
Adult Rats ◽  
Testosterone Metabolism ◽  
Pubertal Maturation ◽  
Immature Rat ◽  
Age Related ◽  
Rat Epididymis ◽  
Old Rats ◽  
Prepubertal Rats ◽  
Cauda Epididymidis

We examined the production in vitro of 5α-reduced metabolites from testosterone by the rat epididymis during pubertal maturation. Minced caput and cauda epididymides from 30-, 45-, and 55-day-old rats were incubated with [3H]testosterone for 2 h. Analysis of the radioactive metabolites revealed both similarities and differences in the metabolic patterns compared to those reported for adult rats. As in adults, 5α-dihydrotestosterone was the most abundant metabolite produced by both epididymal segments at all three ages, and it was formed in larger quantities in the caput epididymidis than in the cauda. However, [3H]testosterone metabolism by the epididymis of the immature rat was characterized by a lower formation of 5α-androstane-3α,17β-diol and higher production of 5α-androstane-3,17-dione than in adults. Production of these two metabolites by the caput region increased and decreased respectively, toward adult levels, with increasing age. In addition, the amount of [3H]testosterone metabolized was higher with tissues from prepubertal rats (30 days of age) than with those from rats 55 days of age. These data suggest that testosterone metabolism in the caput begins to change to that of the adult during the period of pubertal maturation but apparently not until later in the cauda epididymidis.

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