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Biomedical subjects

F Cattabeni

Publications and source records attributed to F Cattabeni.

At least 181 records · Page 10Linked to original sources
PubMed1985

Brain and blood levels of bismuth after oral or parenteral administration of tripotassium-dicitrato bismuthate to rats.

Bismuth levels in blood and brain of rats have been measured following acute or subchronic administration of tri-potassium-dicitrato bismuthate (TDB) by intraperitoneal injection or by gavage. After parenteral administration, the presence of bismuth in blood was associated with appreciable bismuth concentrations in brain of treated animals (approximately equal to 10-30% of blood levels). In contrast, following oral treatment, no bismuth was detected in brain of animals, even at doses of TDB able to produce blood bismuth concentrations comparable with those obtained after intraperitoneal administration. The formation of different bismuth species in blood of treated animals depending upon the route of administration of TDB is suggested.

Administration, Oral↗
PubMed1984

Involvement of arachidonic acid metabolites in beta-adrenoceptor desensitization: functional and biochemical studies.

The prolonged in vitro perfusion of rat lung with isoproterenol (Iso) induced a desensitization of beta-adrenoceptors which was dose- and time-dependent. The decrease in functional responsiveness of rat lung parenchyma to the beta-agonist correlated well with the loss of [3H]dihydroalprenolol ([3H]DHA) binding sites and adenylate cyclase activity after the beta-adrenoceptor desensitization procedure. The cyclooxygenase inhibitor indomethacin prevented the beta-adrenoceptor desensitization as was shown by the restored isoproterenol-induced relaxation in rat lung parenchyma strips and adenylate cyclase activity after the milder desensitization procedure. Inhibition of the arachidonic acid cascade at different levels with different compounds such as BW 755C and betamethasone prevented the desensitization of beta-adrenoceptors. These findings suggest a role for arachidonic acid metabolites in beta-adrenoceptor desensitization. The possible sites of action of arachidonic acid metabolites are also discussed in relation to the inability of indomethacin to prevent the desensitization of beta-adrenoceptors that was induced by the higher Iso concentration used.

Adenylyl Cyclases↗
PubMed1984

Long-lasting tolerance to stimulatory effects of perinatal caffeine treatment.

Pregnant rats were treated with caffeine in their drinking water at doses of 136.3 mg/kg/day during gestation and 222.2 mg/kg/day during lactation. The resulting offspring at 60 days of age (40 days after drug withdrawal) were tested in an activity monitor cage. Spontaneous locomotor activity and that induced by caffeine (10, 30, 60 mg/kg/day) were observed. Treated rats showed apparent tolerance to caffeine-induced motility. Therefore perinatal caffeine treatment seems to induce long-lasting tolerance. This finding contrasts with those previously reported for chronic caffeine treatment in adult rats, where tolerance disappears after only 2-3 weeks following drug withdrawal.

Animals↗
PubMed1984

Loss of intrinsic striatal neurons after methylazoxymethanol acetate treatment in pregnant rats.

Treatment of pregnant rats with methylazoxymethanol (MAM) induces a marked microencephaly in the offspring. The striatum is one of the brain areas affected by treatment. We show that in striatum there is a 30% loss of dopamine (DA)-dependent adenylate-cyclase activity: this indicates that cells bearing type 1 DA receptors are affected by MAM treatment. Moreover, since kainic acid retains its neurotoxic activity, corticostriatal fibers do not seem to be affected, despite the dramatic reduction of cortex size.

Adenylyl Cyclases↗
PubMed1984

Methylazoxymethanol microencephaly in rats: neurochemical characterization and behavioral studies with the nootropic oxiracetam.

The administration of methylazoxymethanol (MAM) to pregnant rats induced a marked reduction in the weight of the offspring's brain. This reduction was due to aplasia of the cortex and hippocampus, whose thicknesses were 50% of those of control animals. A significant reduction was also observed in the striatum. This aplasia could be ascribed to the antimitotic effect of MAM, which, when given at gestational day 15, prevented the development of neurons in the three brain areas mentioned. Indeed, we infer here that the total number of GABA-receptor complexes, as measured by [3H]muscimol and [3H]flunitrazepam binding, was reduced to the same degree as was the weight of the cortex. Similarly, total [3H]haloperidol binding sites were reduced in the striatum. From the behavioral point of view, offspring of MAM-treated rats (MAM rats) showed impaired acquisition in the water-maze and pole-climbing tests, indicating that this brain aplasia had disrupted cognitive processes. In contrast, these animals showed normal growth, and grossly their behavior appeared normal. Oxiracetam, a new compound that belongs to the recently described class of nootropic drugs, was able to restore acquisition processes in MAM rats. We propose therefore that MAM rats might become an interesting and quite simple animal model for evaluation of new acquisition-enhancing drugs. Moreover, this model could also be useful to study the neurochemical correlates of cognitive processes.

Abnormalities, Drug-Induced↗
PubMed1983

Beta-adrenoceptor desensitization in rat lung: functional and biochemical aspects.

Rat lung parenchymal strips were used to study beta-adrenoceptor desensitization from both a functional and a biochemical point of view. Prolonged "in vitro' exposure of rat lung to the beta-agonist isoproterenol (10(-6) M for 20 min) markedly reduced the antagonistic activity of isoproterenol on carbachol-induced contractions. The loss of responsiveness to isoproterenol was associated with a 33% decrease of the beta-receptor number with concomitant reduction of isoproterenol-stimulated adenylate cyclase activity, whereas the enzyme response to NaF was identical in control and in desensitized rat lung. On the basis of these results obtained by comparing the functional and biochemical aspects of the desensitization process, we suggest that the marked reduction of pharmacological activity of isoproterenol after desensitization was primarily due to the decrease in the number of binding sites. The possible molecular mechanisms underlying desensitization are also discussed.

Adenylyl Cyclases↗
PubMed1983

Convulsions induced by lindane and the involvement of the GABAergic system.

The neurochemical changes underlying the convulsant effects of Lindane, an organochlorinated insecticide, are not known. Since electrophysiological and pharmacological data suggest the view that gamma-aminobutyric acid (GABA) plays an important role in controlling convulsive seizures, the effect of lindane on the GABAergic system, on different areas of the rat brain, has been evaluated. Lindane (100 mg/kg i.p.) induces a selective increase of GABA levels in the cerebellum after the onset of seizures. Non-significant increases were observed in the cortex and hippocampus. GABA turnover, as measured by the accumulation rate of GABA after blockade of its catabolism, was increased in all the brain areas examined. On the other hand, lindane does not significantly displace from their binding sites in vitro either 3H-GABA or 3H-Flunitrazepam. These findings show that convulsions elicited by lindane are not due to an impairment of the GABAergic system. Moreover, an increase of GABA functional activity takes place, in all brain areas examined, probably as a protective mechanism to counteract the seizures.

Animals↗
PubMed1983

Behavioural and biochemical effects in the adult rat after prolonged postnatal administration of clozapine.

Rats were administered 10 mg/kg SC of clozapine (C) or vehicle solution (S) daily from day 1 after birth until 20 days of age. At 60 days of age (40 days after the postnatal treatment with C or S was interrupted) the stereotyped behaviour and the effects on locomotor activity elicited by apomorphine in S- and C-pretreated rats were investigated. The intensity of stereotyped behaviour as well as the decrement in locomotion induced by apomorphine (0.5--1 mg/kg SC) were not influenced by chronic C administration during development. Finally, at 80 days of age (60 days after the postnatal treatment with C or S was interrupted) rats were subjected to a differential reinforcement of low rates schedule (DRL15s). The results indicate that the acquisition of the DRL task performance criterion (Rs/Rf less than or equal to 2.5) was significantly more rapid in S-pretreated rats than in C-pretreated ones. In parallel biochemical experiments, homovanillic acid (HVA) content was measured in striatum in rats at 60 days of age (40 days after the postnatal treatment with C or S was interrupted). The results indicate that even if an acute challenge dose of 10 mg/kg C shows a certain degree of tolerance a single dose of 20 mg/kg C is still able to increase striatal HVA concentration in chronic C-pretreated animals. These data indicate that early postnatal administration of a non-cataleptogenic neuroleptic, like C, induces, in the adult rat, behavioural and biochemical changes which significantly differ from those elicited by a cataleptogenic neuroleptic, like haloperidol.

Animals↗
PubMed1983

Early postnatal chlordiazepoxide administration: permanent behavioural effects in the mature rat and possible involvement of the GABA-benzodiazepine system.

The long term behavioural and biochemical effects of chronic chlordiazepoxide treatment during the period of neuronal maturation in the rat have been investigated. The administration to lactating mothers of chlordiazepoxide at very low doses (0.22 and 2.6 mg/kg) in their drinking water affects both behavioural and biochemical parameters in offspring at 60 days of age and undrugged since weaning. A deficit in the acquisition of the conditioned avoidance response in treated rats was observed, although no significant difference in spontaneous locomotor activity between control and treated rats was found. 3H-Flunitrazepam binding sites in cerebral cortex and hippocampus were decreased by the treatment, whereas no change was detected in cerebellum. Moreover, 3H-muscimol binding sites increased in hippocampus with no changes in cerebral cortex and cerebellum. According to the different regional distribution of benzodiazepine type 1 and type 2 receptors, we suggest that type 2 receptors are selectively affected by the treatment, and that the GABAergic receptor system is also permanently altered by administration of chlordiazepoxide during early postnatal life.

Animals↗
PubMed1983

The influence of early postnatal treatment with haloperidol on the effects induced by small and large doses of apomorphine on locomotion of adult rats.

Chronic administration of haloperidol (0.5 mg/kg, s.c.) during early postnatal life did not modify the effects produced by a small dose of apomorphine (0.02 mg/kg, s.c.) on the locomotor activity of adult rats; conversely, the reduction of locomotion induced by a large dose of apomorphine (1 mg/kg, s.c.) was much more kared in haloperidol-pretreated rat than in saline-pretreated ones. The differential ontogeny of dopamine auto- and postsynaptic receptors could be partly responsible for the different influence of postnatal treatment with haloperidol on the responsiveness of the adult to small and large doses of apomorphine.

Animals↗
PubMed1983

Endogenous gamma-hydroxybutyrate in rat brain areas: postmortem changes and effects of drugs interfering with gamma-aminobutyric acid metabolism.

The possibility that gamma-hydroxybutyrate (GHB), a metabolite of gamma-aminobutyric acid (GABA), may play a role in the CNS has recently come to attention. We describe here a sensitive and specific mass fragmentographic technique that allows the measurement of picomole amounts of GHB in single rat brain areas. Moreover, we show that GHB can accumulate postmortem, an effect that is blocked by the use of microwave irradiation to kill the animals. To understand further the relationship between GABA and GHB formation, we treated rats with drugs known to interfere with GABA metabolism at different levels and concomitantly measured GABA and GHB in cerebral cortex and cerebellum. Isoniazide, which blocks the formation of GABA, also decreases GHB. Blockers of the catabolism of GABA, such as aminooxyacetic acid and gamma-acetylenic GABA, increase GABA levels and decrease those of GHB. Sodium dipropylacetate increases both GABA and GHB, supporting the hypothesis that this effective antiepileptic drug also blocks in vivo the enzyme that converts succinic semialdehyde to succinic acid.

Alkynes↗
PubMed1981

Enduring behavioural and biochemical effects in the adult rat after prolonged postnatal administration of haloperidol.

Rats were administered 0.5 mg/kg SC of haloperidol (H) or saline (S) daily from day 1 after birth until 20 days of age. At 60 days of age (40 days after the postnatal treatment with H or S was interrupted) the stereotyped behaviour and the effects on locomotor activity elicited by apomorphine in S- and H-pretreated rats were investigated. The intensity of apomorphine (0.5--1 mg/kg, SC)-induced stereotyped behaviour was significantly greater in the H-pretreated group than in S-pretreated animals and this was accompanied by a much more marked reduction of locomotor activity in H-pretreated than in S-pretreated rats. Finally, at 80 days of age (60 days after the postnatal treatment with H or S was interrupted) rats were subjected to a Differential Reinforcement of Low Rates schedule (DRL 15-s). The results indicate that the acquisition of the DRL task performance criterion (Rs/Rf less than or equal to 2.5) was significantly more rapid on S-pretreated rats than in H-pretreated ones. In parallel biochemical experiments, acute H produced smaller increases in dopamine turnover in chronic H-treated rats compared with S-treated controls. These data indicate that H treatment in neonatal rats induces behavioural and biochemical changes which can be observed up to 60 days after H withdrawal.

3,4-Dihydroxyphenylacetic Acid↗