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Biomedical subjects

U Scapagnini

Publications and source records attributed to U Scapagnini.

At least 163 records · Page 9Linked to original sources
PubMed1969

Brain monoamines and adrenocortical activation.

1. The effect of a pharmacologically induced increase or depletion of brain monoamines (5-hydroxytryptamine, noradrenaline, dopamine) was investigated with respect to adrenocortical function.2. No strict correlation was found between the depletion of brain amine stores induced by prenylamine or p-chlorophenylalanine and adrenocortical activation, even at times in which the peak effect of brain amine depletion occurs.3. Restraint stress causes a manifest increase in brain 5-hydroxytryptamine while decreasing the cerebral noradrenaline and dopamine content. This stress strongly stimulates corticosterone secretion by the adrenals.4. A monoamine oxidase inhibitor, nialamide, at a dose which causes an evident increase in brain amine concentrations, does not modify plasma corticosterone. At the same dose it was, furthermore, unable to prevent the adrenocortical stimulation induced by restraint stress.5. Brain amine content does not seem to play an important part in the control of corticotrophin releasing factor in corticotrophin secretion by the pituitary gland. The relationship between hypothalamic monoamines and other neurohumours is discussed.

Adrenal Glands↗
PubMedDate not supplied

Phosphatidylserine counteracts physiological and pharmacological suppression of humoral immune response.

Phosphatidylserine (PS) is a necessary cofactor for protein kinase C (PKC) activation, and changes in the synthesis of PS have been shown to participate in the mechanism(s) involved in the transmembrane signaling of interleukin 1 (IL-1). In view of the age-associated defects in T-cell functions, in the present study we have addressed the question of whether an in vivo treatment with PS might interfere with such processes. Furthermore, the effect of an in vitro treatment with PS in human peripheral blood monocytes (PBMC) or splenocytes activated with a lectin mitogen, on the expression of IL-2 receptor, was assessed. While the process of ageing was accompanied by a marked decline of humoral response monitored by anti-BSA antibodies (of the IgG class) production, following immunization with BSA in complete Freund adjuvant, chronic treatment with PS (50 mg/kg, in drinking water), reversed this effect, raising specific antibody titers to levels practically indistinguishable from those measured in young animals. Pharmacological depression of humoral immune response induced by a treatment of adult animals with dexamethasone was similarly reversed by a chronic treatment with PS. While only a pharmacological concentration (10(-5) M) of PS significantly increased IL-2 receptor expression in activated human PBMC, simultaneous treatment of PBMC with inactive doses of PS and the pharmacological activator of PKC (phorbol myristate acetate, PMA, 10(-8) M) resulted in a synergistic stimulation of Tac+ cells. Furthermore, in cultures of rat splenocytes PS (10(-6) M) significantly stimulated the expression of IL-2 receptor, and concomitant addition of PS (10(-7) M) to Con A-stimulated splenocytes produced a significant potentiation of IL-2 receptor induction. The present results indicate that in vivo treatment of ageing animals with the specific phospholipid PS is able to reverse the physiological decline of the humoral immune response induced by the ageing process. Moreover, treatment of young rats with PS reversed the pharmacological associated depression of specific antibody production. The in vitro effects of the phospholipid on human PBMC and rat splenocytes might suggest that PS is implicated in T-cell activation through its action on IL-2 receptor.

Aging↗
PubMedDate not supplied

Protective action of phosphatidylserine on stress-induced behavioral and autonomic changes in aged rats.

Phosphatidylserine (PS) was administered in aged rats subjected to various stressor stimuli in order to evaluate its effect on grooming behavior, core temperature and gastric ulcers. Novelty-induced grooming appeared to be increased in aged rats as compared to young controls. The subchronic intraperitoneal treatment with PS (20 mg/kg/day for 20 days) decreased grooming activity in aged rats, whereas it did not affect that of young animals. Restraint stress induced hyperthermia in both aged and young rats. However, 90 min after the beginning of restraint, PS-treated old rats showed a normalization of core temperature. Furthermore, restraint-plus-cold stress induced gastric ulcers in both aged and young rats. The treatment with PS was followed by a decreased incidence of gastric lesions in aged, but not in young rats. The mechanism of PS protective action against stress-induced behavioral and autonomic changes is unknown, but it may involve the brain level as this drug exerts a noteworthy influence on behavior and autonomic functions.

Aging↗
PubMedDate not supplied

Effects of RGH 2202 on cognitive and motor behavior of the rat.

The behavioral activity of the thyrotropin-releasing hormone (TRH) analogue, L-6-ketopiperidine-2-carbonyl-leucyl-L-prolinamide (RGH 2202), has been studied in animal models of central neurotransmission disruption. In 24-month-old rats, repeated administration of the peptide (5 or 10 mg/kg/day, injected IP for 20 days) was followed by a facilitated acquisition of active avoidance behavior in the shuttle-box test and retention of passive avoidance reaction in a step-through passive avoidance task. Also, ambulation in an open field was increased and motor performance and co-ordination in the rotorod test was facilitated by the treatment. Scopolamine-induced amnesia was reverted by RGH 2202 in adult rats tested both in active and passive avoidance tasks. Cognitive deficits induced in rats by prenatal manipulation with methylazoxymethanol (MAM) were reduced in adulthood by repeated administration with RGH 2202. These results indicate that the TRH-analogue, RGH 2202 may improve cognitive and motor disturbances in aging or induced by central neurotransmission disruption. It is possible that the peptide is functioning, at least in part, by intervening with the central cholinergic neurotransmission.

Age Factors↗
PubMedDate not supplied

Dihydroergocryptine improves behavioral deficits of aged male rats.

Dihydroergocryptine (DHECP), an ergot alkaloid with potent dopaminergic activity, was injected acutely or subchronically to aged (24 months old) male rats of the F344 strain, at the dose of 0.05 or 0.1 mg/kg. The immobility in the "despair" test (constrained swim) was longer in 24-month-old rats than in younger animals. This behavioral change was reduced in rats treated subchronically with DHECP, but no significant change was found in animals with acute treatment. Aged rats showed an increased haloperidol-induced catalepsy and a reduced motor performance and coordination as compared to animals of 2 and 10 months of age. Acute treatment with DHECP was followed by an attenuation of haloperidol-induced catalepsy and an improvement of motor performance and coordination of aged rats. Similar results were obtained after subchronic treatment with DHECP, but the effect on the rotorod behavior was more potent after subchronic treatment than after acute injection of the drug. It is possible that the improvement of behavioral deficits of aged rats after the treatment with DHECP depends on the facilitating effect of this drug on central dopamine transmission that may be impaired in these animals.

Aging↗
PubMedDate not supplied

Radioprotective effects of the association thymopentin-interleukin-1 alpha in the C57BL/6 mouse.

We investigated whether thymopentin, a synthetic pentapeptide derivative of thymopoietin, could enhance the protective effect of interleukin-1 alpha when both administered prior to sublethal irradiation in the C57BL/6 mouse. Thymopentin (10 mg/kg/day/7 days) was injected intraperitoneally in groups of C57BL/6 mice. Then, interleukin-1 alpha was administered on day 7. Twenty hr later, all groups were given whole body sublethal irradiation of 750 rad by 60Co elements. In some groups of mice, treatment with thymopentin was continued for 1 week after irradiation. Efficacy of the combination treatment was assessed by evaluation of mortality, as well as by histologic examination of the brain, testis, bone marrow, heart and spleen. The combination of relatively low doses of interleukin-1 alpha (700 U) with thymopentin yielded a survival which was nearly that observed with interleukin-1 alpha (1000 U) given alone (about 100%). The optimal effect was observed in animals treated for 15 days with thymopentin, either in combination or alone. In addition, incidence and severity of histological lesions were also lower in animals with the some treatment schedule. Our results suggest that the combined treatment thymopentin-interleukin-1 alpha prevents radiation damage in the mouse.

Animals↗