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G Calderini

Publications and source records attributed to G Calderini.

At least 19 recordsLinked to original sources
PubMed1990

Hyaluronic acid prevents oxygen free-radical damage to granulation tissue: a study in rats.

Oxygen free-radicals are known to impair wound healing after ischaemia-reperfusion or polymorphonuclear cell stimulation. Furthermore, they reduce the breaking strength of all recent wounds and might be a cause of wound leakage. This study was performed to evaluate whether or not hyaluronic acid can reduce the risk of wound impairment caused by free-radicals, in rats with abdominal sepsis, polymorphonuclear cell stimulation or cytochrome C function derangement produced by xenobiotics. Male Sprague-Dawley rats with open wounds received phenazine methosulfate or zimosan, or had abdominal sepsis to induce oxygen free-radical generation. There were three groups of treatment: hyaluronic acid cream, hyaluronic acid ethyl ester gel, and placebo. The reduction in wound size was measured from the 1st to the 11th postoperative day; biopsies were taken for histological evaluation. Every other day, a gentle debridement was performed in all the groups of animals. We found that hyaluronic acid and its ethyl ester derivative significantly improved the wound healing of rats subjected to an increased generation of oxygen free-radicals. It remains to be established whether or not hyaluronic acid acts as a scavenger of free-radicals.

Animals↗
PubMed1987

Developmental and age-related changes in D1-dopamine receptors and dopamine content in the rat striatum.

The relationship between the postnatal development of dopaminergic (DAergic) nerve endings and the maturation of D1 DA receptors in the rat striatum was analyzed by measuring the content of DA and dihydroxyphenylacetic acid (DOPAC), two biochemical markers of DAergic nerve terminal proliferation, and the ontogenetic changes in [3H]SCH 23390 binding sites. DA-stimulated adenylate cyclase (AC) activity was also measured in order to characterize the coupling of [3H]SCH 23390 binding sites to the responses mediated by the activation of D1 DA receptors. Striatal levels of DA and DOPAC, as well as the density and affinity of [3H]SCH 23390 binding sites and DA-stimulated AC activity were also measured in senescent rats. The striatal content of DA increased slowly after birth, reaching adult levels by postnatal day 60 and remaining constant through adulthood and senescence (up to 20 months of age). The density of [3H]SCH 23390 binding sites increased 14-fold from birth to postnatal day 35, when a peak value was reached, whereas a significant decrease was observed in the striatum of aged rats. In contrast, the affinity of D1 DA receptors for [3H]SCH 23390 remained unchanged from birth through senescence. The stimulation of cyclic AMP formation induced by 100 microM DA increased 4-fold from birth to postnatal day 14, when the maximal responsiveness to DA was observed and then returned to adult levels. No significant alterations were observed in the Km values during development, whereas the stimulatory effect of 100 microM DA on AC activity was significantly decreased in senescent rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Age-dependent changes in the mechanisms controlling prolactin secretion and phosphatidylinositol turnover in male rats: effect of phosphatidylserine.

The present study was undertaken in order to better characterize the functional state of anterior pituitary gland in young and old rats by using prolactin secretion and incorporation of radioactive phosphate into phosphatidylinositol (PI) as markers. The in vitro incorporation of radiolabeled phosphate into anterior pituitary PI was significantly (p less than 0.01) greater in young (3-5 months) than in aged (24-25 months) male Sprague-Dawley rats. No significant difference was found in the incorporation by pituitary tissue of 32P into phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Also, the extent of prolactin secretion from isolated pituitary was significantly greater in young than in aged rats, while the prolactin pituitary content was significantly higher in aged animals. In vitro dopamine (DA) decreased the incorporation of 32P into PI, both in young and old pituitary glands, and inhibited prolactin secretion into the incubation medium. Brain cortex-phosphatidylserine (BC-PS), a pharmacologically active purified phospholipid, capable of stimulating the dopaminergic system in the hypothalamus and of decreasing prolactin secretion both in humans and rats in vitro and in vivo, inhibited the incorporation of labeled phosphate into PI of pituitary glands from either young or old rats, but did not alter the prolactin secretion from the glands incubated in vitro. Baseline prolactin plasma levels did not differ significantly between young and old rats either when blood was collected from the trunk after decapitation or underwent sampling from chronically cannulated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1987

Reparative processes in aged brain.

Endogenous neurotrophic factors have been proposed to play an important role in degenerative diseases and aging. In aged rats, neurotrophic activity induced by partial lesion of nigro-striatal pathways seems to be lower compared to young rats when assayed in vitro on cultured mesencephalic dissociated neuronal cells. In parallel experiments, we could also observe an age-dependent delay in spontaneous recovery of striatal tyrosine hydroxylase activity after lesion. Both experimental evidences suggest a low-potential neuroplasticity in aged rats. Nevertheless, the aging brain seems to be responsive to pharmacological manipulation. Long-term phosphatidylserine treatment has been shown to maintain the integrity of neuronal structures altered by the aging process. Putative mechanisms of action underlying these effects are presented.

Aging↗
PubMed1986

Turnover of palmitic and arachidonic acids in the phospholipids from different brain areas of adult and aged rats.

[3H]Palmitic acid and [14C]arachidonic acid were injected together into the cerebral ventricle of 4-month and 24-month-old rats. At different time intervals from the injection, the distribution of these fatty acids in the lipids from different brain areas was examined. The fatty acids were rapidly incorporated into the lipids through different mechanisms. The time-specific activity relationship indicate that the utilization of the fatty acid differs according to the different areas and aging decreases the utilization of both the fatty acids. The decline of arachidonic acid incorporation into phospholipids is particularly evident, indicating that aging affects mainly the utilization of polyunsaturated fatty acids.

Aging↗
PubMed1986

Phorbol 12-myristate 13-acetate induces prolactin secretion from rat anterior pituitary gland by the activation of protein kinase-C.

The purpose of this study was to characterize the action of phorbol 12-myristate 13-acetate (PMA), a tumor-promoting agent, on rat anterior pituitary gland, focusing the attention on prolactin secretion. PMA elicited a significant increase in prolactin secretion without affecting phosphatidylinositol turnover, considered as an early post-receptor event controlling PRL secretion. However incubation of anterior pituitary glands with PMA caused a loss of protein kinase-C activity in cytoplasm concomitant with an increased enzyme activity in the membrane. The action of PMA on prolactin secretion seems to be mainly dependent from the redistribution and activation of protein kinase-C. In fact, the phorbol ester did not affect pituitary cAMP and cGMP metabolism either in basal conditions or after theophylline.

Animals↗
PubMed1985

Experimental models of aging and quinolinic acid.

The normal aging process results in many functional deficits in which the central nervous system (CNS) plays a primary role. However, the study of brain aging involves numerous difficulties, including not only the complex anatomical and functional organization of the brain itself, but also because the length of the experiments themselves and experimental costs are often crucial limitations. This highlights an ever increasing need for the development of alternative model systems capable of mimicking at least to some degree the main alterations observed during the normal aging process. A comparative study of electrophysiological and behavioural features in aged rats and in young rats following chronic administration of a naturally occurring brain metabolite, quinolinic acid (QUIN), recently demonstrated to increase in the cerebral cortex of rats as a function of age, is reported. In rats there occurs an age-dependent increase in the number of animals displaying spontaneous asymptomatic spike-wave discharges, associated with impaired performance in the passive avoidance test. Chronic oral administration of QUIN to young rats also results in cortical spiking activity, without any detectable neuronal cell damage at cortical or hippocampal levels, associated with behavioural deficits similar to those observed in old rats. The utilization of young, QUIN-treated animals may thus perhaps offer an alternative model system for the comprehension of the mechanisms involved in some age-related functional impairments.

Aging↗
PubMed1985

Serine phospholipids and aging brain.

For many years phospholipids have been studied mainly for their possible use as membrane models or cell-like carriers. Recently, on the basis of the new knowledge on the phospholipid membrane structure and function, a novel interest has arisen on the pharmacological properties of these compounds particularly at cerebral level. In this context particular attention has been devoted to phosphatidylserine (BC-PS), an anionic phospholipid extracted and purified from bovine brain, which in young animals has been shown to modify a number of brain electrophysiological and biochemical parameters.

Aging↗
PubMed1985

Effect of chronic treatment with phosphatidyl serine on phospholipase A1 and A2 activities in different brain areas of 4 month and 24 month old rats.

The activities of phospholipase A1 and A2 were tested in mitochondria and microsomes from different cerebral areas of both 4 month and 24 month old rats, after 30 days i.p. treatment with ox Brain Cortex Phosphatidyl Serine (BC-PS). In the brain areas from control animals a rather great decline in its ability to hydrolize the fatty acids of the main phosphoglycerides was found. Taking into account only the effect of treatment with BC-PS on the modification of phospholipase activities caused by aging, we found that the treatment was able to balance the enzymatic functions altered by aging in several of the area examined. The importance of this result on the lipidic metabolism of the aging brain is also discussed.

Aging↗
PubMed1984

Depletion and recovery of neuronal monoamine storage in rats of different ages treated with reserpine.

The effect of reserpine on dopamine, noradrenaline, adrenaline and serotonin concentrations in different brain regions, and the recovery of normal levels of these monoamines after such treatment were studied in rats aged 5, 15 and 27 months. In a preliminary experiment we found that distribution of the drug was not altered in the aged rats. Then we observed that a single dose of reserpine (5 mg/kg IP) had a similar depleting effect on all the brain monoamines, in all the brain regions considered in all three age groups. The curves expressing recovery of monoamine storage in all the nerve terminals, several days after treatment, were superimposable. These results suggest that in the rat, age does not influence the effect of reserpine on the storage mechanism of brain monoamines. Moreover, as restoration of this mechanism depends on the synthesis of new vesicles, the similarity in the rates of recovery in adult, old and very old rats indicated indirectly that synthesis of these neuronal organelles is not affected by aging.

Aging↗
PubMed1983

Calmodulin content in different brain areas of aging rats.

An age-related decrease of calmodulin content was detected in the striatum, cerebral cortex and cerebellum of 3-, 22- and 30-month-old rats. This age-related decrease of calmodulin level occurred both in the supernatant and in the pellet fraction of high speed centrifuged tissues. However, the rates of age-dependent calmodulin loss in the pellet and supernatant fraction were differentiated according to the cerebral region considered, suggesting a different brain area sensitivity to the aging process.

Age Factors↗
PubMed1983

Biochemical changes of rat brain membranes with aging.

Modification of membrane composition and enzymatic activities both in total brain homogenate and purified synaptic plasma membrane of 3 and 24 month old rats has been investigated. Protein, cholesterol and phospholipid content and (Na+, K+)ATPase and 2',3' cyclic nucleotide phosphohydrolase activities were determined. The major changes occurred in the whole homogenate where a general increase in total protein and cholesterol content with age and a significant increase of the cholesterol/phospholipids molar ratio has been detected. In S.P.M. aging process induced a decrease of protein, cholesterol and phospholipids content associated with an increased membrane viscosity and a decrease of delta E. These data are consistent with a change in the structural organization and in the distribution pattern of different cell population in the aging brain. A possible artifactual effect of freezing on the reported parameter is also discussed.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1983

Temporal sequence of changes in central noradrenergic system of rat after prolonged antidepressant treatment: receptor desensitization and neurotransmitter interactions.

It has been shown that different receptor components may be involved in the adaptive changes occurring in noradrenergic (NE) neurones after prolonged periods of exposure to antidepressant drugs. In this report the desensitization of NE-coupled adenylate cyclase (NE-AC). beta-adrenergic receptors and [3H]imipramine ([3H]-IMI) or [3H]desipramine ([3H]-DMI) binding sites have been temporally correlated with in vivo changes of NE utilization. Normetanephrine (NMN) was measured as indicator of NE synaptic events involved in antidepressant action. Concentrations of normetanephrine were increased after acute desipramine (DMI), viloxazine and mianserin administration. Following 3 days of treatment, the antidepressant-induced increase of normetanephrine became tolerant and NE neurones were resistant to the antidepressant effect until the 15th day of treatment. After two weeks, DMI elicited a significant decrease in the content of normetanephrine. A different pattern of changes has been found in the temporal modification of [3H]-IMI recognition sites, beta-adrenoceptors and NE-AC activity after chronic DMI treatment. Binding sites and receptors were down regulated after 10 days of treatment preceding the decrease in normetanephrine content. No down-regulation was observed in [3H]-DMI binding sites. Studies on the effects of antidepressants during brain maturation revealed that the mechanisms which cause desensitization of beta-receptors and [3H]-IMI binding sites appear in the early stages of postnatal life. Since [3H]-IMI and [3H]-DMI recognition sites have been shown to be located on serotonergic (5-HT) and noradrenergic neurones respectively, the interactions between NE and 5-HT neurones could represent possible mechanisms implicated in receptor desensitization. The experiments presented involving lesions of 5-HT neurones have clearly demonstrated that NE release in rat cerebral cortex is under a tonic serotonergic influence. Alterations in the chemico-physical properties of the synaptic membranes might be also taken in consideration for the mechanisms underlying receptor modulation. In fact, evidence is provided that in neural tissue phospholipid methylation can be affected. In conclusion, the temporal sequence of changes in cortical noradrenergic neurones, after chronic antidepressant treatment, has demonstrated that integrated mechanisms are operative for the function of the overall system.

Animals↗
PubMed1983

Phospholipid methylation increases [3H]diazepam and [3H]GABA binding in membrane preparations of rat cerebellum.

The effect of phospholipid methylation on both [3H]diazepam and [3H]GABA ( [3H]gamma-aminobutyric acid) binding to crude synaptic plasma membrane from rat cerebellum has been studied. S-Adenosylmethionine (SAM) stimulates [3H]methyl group incorporation into membrane phospholipids and enhances [3H]diazepam binding by increasing the apparent Bmax. Conversely, inhibition of [3H]methyl group transfer from [3H]SAM to phospholipids by preincubation with SAM at 0 degrees C or with SAH abolishes the increase of binding. After preincubation with SAM, analysis of the GABA binding reveals the presence of binding sites with high affinity, a property absent in control membranes preincubated without SAM. Among the neurotransmitter bindings tested, only those of GABA and benzodiazepine in the cerebellum and beta-adrenergic ligands in the cerebral cortex are enhanced upon stimulation of phospholipid methyltransferase activity. [3H]Dihydromorphine, [3H]dihydro-alpha-ergokryptine and [3H]spiroperidol bindings are not affected by SAM. The present data suggest an involvement of phospholipid methylation in regulation of both [3H]GABA and [3H]-diazepam binding.

Animals↗
PubMed1982

Age-related changes of benzodiazepine and GABA binding sites in the rat retina.

The changes in the number and sensitivity of benzodiazepine and GABA binding sites in the rat retina during postnatal development, adulthood and ageing and their functional relationship at different ages have been studied. Data indicate an increase in the total number of both GABA and benzodiazepine binding sites with age. In contrast, the activation of retinal benzodiazepine receptor binding by GABA is significantly reduced in aged rats with respect to young adult and newborn rats. Moreover, the activation of retinal benzodiazepine receptor binding induced by dark exposure of the animals is present in young adult rats but is lost in aged rats. These results suggest that in the retina of aged rats there is an increase of GABA and benzodiazepine receptors which have lost their functional connection.

Aging↗
PubMed1982

Changes with age in rat central monoaminergic system responses to cold stress.

Changes with age in responses to stress of certain central monoaminergic systems were investigated. Three groups of rats, 4, 18 and 29 months old, were exposed to cold and the effect of this stress on hypothalamic tyrosine hydroxylase, and on the metabolism of DA and 5HT in different brain regions was evaluated. Senescent rats were unable for several hours to compensate the loss of body heat. Corticosterone secretion however was equally stimulated. Hypothalamic tyrosine hydroxylase activity was enhanced in the young rats but not in the old ones. However, the two groups of senescent rats did not show the increase in HVA levels noted in striata of young rats 2 hours after cold exposure. In contrast, the 18 and 29-month-old rats presented enhanced serotonergic tonus, indicated by the greater increase in 5HIAA determined by stress.

Aging↗
PubMed1982

Changes in monoamines and their metabolite levels in some brain regions of aged rats.

The concentrations of dopamine (DA) norepinephrine (NE), serotonin (5HT) and their metabolites, HVA, DOPAC, MHPG-SO4 and 5HIAA were measured in several brain areas of rats aged 4, 18 and 29 months. Dopamine and its metabolites showed a decline, statistically correlated with age, in all the dopaminergic areas considered, indicating that this system is profoundly affected in the senescent rat. The changes in the noradrenergic system were more complex. This neurotransmitter was reduced in spinal cord and in limbic area, but was not modified in hippocampus, cerebellum, striatum and s. nigra. In cortex, MHPG-SO4, the main NE metabolite, showed a significantly age-related increase. Tyrosine hydroxylase (TH) activity was low in striatum, and brainstem but not in hypothalamus of aged rats. Neither 5HT nor its metabolites was affected by age. The results indicate that central catecholaminergic systems are markedly affected in senescent rats.

3,4-Dihydroxyphenylacetic Acid↗