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M Sansone

Publications and source records attributed to M Sansone.

At least 37 records · Page 2Linked to original sources
PubMed1992

Oxiracetam prevents haloperidol-induced passive avoidance impairment in mice.

The nootropic drug oxiracetam (50 mg/kg) prevented passive avoidance impairment induced by posttraining administration of haloperidol (0.25 and 0.5 mg/kg). Conversely, oxiracetam did not antagonize either locomotor depression or suppression of active avoidance responses induced by the dopamine receptor blocking agent. The results indicate that prevention of haloperidol-induced retention impairment, by oxiracetam, may be due to a not yet defined protective action, common to other nootropic agents, on different types of experimental amnesias, rather than to a specific interaction with dopaminergic mechanisms.

Animals↗
PubMed1992

Similar effects of nifedipine and hydralazine on anaesthesia and hypermotility induced by pentobarbitone in mice.

Nifedipine, a dihydropyridine calcium channel blocker, and hydralazine, a non-calcium channel antagonist vasodilatator, enhanced pentobarbitone-induced sleeping time and reversed locomotor hyperactivity induced by a subhypnotic dose of the barbiturate in mice. The similarity of the behavioural effects, exerted by nifedipine and hydralazine, suggest that haemodynamic factors may play an important role in the interaction of calcium channel antagonists with barbiturates.

Anesthesia↗
PubMed1992

Nifedipine-morphine interaction: a further investigation on nociception and locomotor activity in mice.

Nociception and locomotor activity were tested in mice (C57BL/6 and DBA/2 strains), receiving the dihydropyridine calcium-channel blocker nifedipine, alone or combined with morphine. The calcium antagonist did not change the reaction time to thermal stimulation (tail-flick test), when administered alone, but combinations of nifedipine and morphine prolonged tail-flick latencies less than did the opiate alone. Nifedipine decreased locomotion in both strains, reduced the hypermotility induced by morphine in C57 mice, and enhanced the locomotor depression induced by the opiate in DBA mice. A comparison of the effects of nifedipine with those of the non-calcium antagonist vasodilator, hydralazine, suggests that the interactions with morphine were not exclusively related to neuronal changes produced by calcium channel blockade, but also to haemodynamic factors. In fact, except for the lack of interference with morphine-induced hypermotility in C57 mice, hydralazine, given alone or in combination with morphine, produced effects similar to those of nifedipine.

Animals↗
PubMed1991

A copper-thiolate polynuclear cluster in the ACE1 transcription factor.

ACE1 is the transcriptional activator of the metallothionein (CUP1 locus) gene in Saccharomyces cerevisiae. Previous data had implicated the N-terminal domain of ACE1 as responsible for the Cu-dependent specific DNA binding. An expression system in Escherichia coli was constructed to enable the isolation of an ACE1 domain containing the DNA and Cu-binding regions. Here we report the purification and characterization of the Cu-ACE1 truncated molecule. Spectroscopic techniques showed that ACE1 contains an unusual type of DNA binding structure that is based on a polynuclear Cu(I)-cysteinyl thiolate cluster. The cluster consists of six or seven Cu(I) ions coordinated to cysteinyl thiolates in a trigonal geometry distorted from planarity. The Cu(I)-cysteine cluster of Cu-ACE1 exhibits structural properties analogous to the Cu(I)-thiolate polynuclear cluster in yeast Cu-metallothionein itself, suggesting an unusual mechanism for the evolution of this regulatory factor. The Cu cluster organizes and stabilizes the conformation of the N-terminal domain of ACE1 for specific DNA binding.

Amino Acid Sequence↗
PubMed1991

Effects of oxiracetam-nicotine combinations on active and passive avoidance learning in mice.

Tested alone, in CD-1 mice, the nootropic drug oxiracetam (50 mg/kg) improved learning in a multitrial active avoidance task (shuttle-box), but did not affect one-trial passive avoidance acquisition. Nicotine, which was ineffective at the dose of 0.25 mg/kg, improved both active and passive avoidance at the dose of 0.5 mg/kg; 1 mg/kg nicotine still exerted facilitating effects on passive avoidance, but slightly depressed shuttle-box performance. Combinations of oxiracetam and nicotine improved passive avoidance more than either drug given separately. In the active avoidance task, a combination of oxiracetam with the lower dose of nicotine exerted improving effects never observed with nicotine alone, even at higher doses. The nootropic drug also prevented the slight depressant action exerted by 1 mg/kg nicotine. Thus, contrary to what was previously supposed, at least in mice subjected to shuttle-box avoidance training, nicotinic activation does not appear as the main neurochemical mechanism involved in the action of oxiracetam. Perhaps, oxiracetam and nicotine activate different types of cholinergic mechanisms, but it cannot be excluded that other neurotransmitters, particularly catecholamines, may be involved in the avoidance facilitating effects produced by nicotine and by combinations of the two drugs.

Animals↗
PubMed1991

Avoidance learning during antidepressant withdrawal in mice.

Shuttle-box avoidance acquisition, locomotor activity and density of adrenoreceptors in the cerebral cortex have been evaluated, in CD-1 mice, during withdrawal from repeated treatment with desipramine or mianserin (5 or 14 daily injections of antidepressant drug, 10 mg kg-1). Withdrawal from mianserin did not produce any behavioural or neurochemical change. Mice withdrawn from desipramine exhibited avoidance facilitation, when training started 24 h (but not 72 or 120 h) after the last injection. Locomotor activity was not affected and no change was found in the density of beta-adrenoreceptors. An up-regulation of alpha 2- and, to a lesser extent, of alpha 1-adrenoreceptors, occurred 72 h following desipramine withdrawal. However, the assessment of the role played by these neurochemical changes in the avoidance facilitation observed during withdrawal from the antidepressant treatment requires further study.

Animals↗
PubMed1990

Oxiracetam prevents mecamylamine-induced impairment of active, but not passive, avoidance learning in mice.

The nicotinic antagonist mecamylamine (2.5 and 5 mg/kg/IP) depressed both active (shuttle-box) and passive (step-through) avoidance learning in mice of the DBA/2 strain. The nootropic drug oxiracetam (50 and 100 mg/kg/IP) improved acquisition in the multitrial active avoidance test, but had no effect on one-trial passive avoidance learning. When the two drugs were combined, oxiracetam did not counteract mecamylamine-induced impairment of passive avoidance learning, even if it maintained a facilitating action on shuttle-box avoidance acquisition in mice receiving the nicotinic receptor blocker. Prevention of mecamylamine-induced shuttle-box avoidance depression by oxiracetam indicates that central nicotinic mechanisms are probably involved in the improving effects exerted by nootropic drugs on learning.

Animals↗
PubMed1989

Pentobarbital-induced hyperactivity in mice: negligible role of opioid mechanisms.

Subhypnotic doses (10 and 20 mg/kg) of pentobarbital significantly elevated locomotor activity measured for 30 min in CD-1 mice. The hyperactivity was also observed in mice recovering from pentobarbital-induced (50 mg/kg) sleep (measurements starting 15 min after recovery of righting reflex). Naloxone in doses up to 4 mg/kg did not affect significantly the pentobarbital-induced hyperactivity in any experiment; a dose of 8 mg/kg only partially attenuated the hyperactivity induced by a dose of 20 mg/kg of pentobarbital, but did not affect significantly either the stimulatory effect of a low subhypnotic dose (10 mg/kg) or the posthypnotic hyperactivity. This suggests a negligible involvement of opioid mechanisms in the hyperactivity induced by pentobarbital.

Animals↗
PubMed1989

Avoidance facilitation by nootropics.

1. The effects on avoidance acquisition of two nootropic drugs, oxiracetam and piracetam, were tested in mice subjected to five daily 100-trial training sessions in the shuttle-box. 2. Oxiracetam (25 or 50 mg/kg/i.p.) and piracetam (100 mg/kg/i.p.), given before each daily session, improved avoidance acquisition in the good performing BALB/c more than in the poor performing C57BL/6. In both cases avoidance facilitation was evident only if training was preceded by a five-day pretreatment. 3. Combinations of nootropics and methamphetamine increased avoidance responses in C57BL/6 mice more than drugs given separately. Conversely, no interaction occurred in a locomotor activity test. 4. Interactive effects in the learning situation, but not in a test of general activity, were also found when oxiracetam was combined with the anticholinergic agent scopolamine. 5. On the whole, the above results demonstrate facilitation of active avoidance acquisition by piracetam-like nootropic agents, but the neurochemical mechanisms involved in this action are not yet clear.

Animals↗
PubMed1989

Suppression of pentobarbitone-induced hyperactivity by past experience in mice.

Locomotor activity of CD-1 mice, tested in an unfamiliar environment (toggle-floor box), was increased either by a subhypnotic dose (20 mg kg-1) of pentobarbitone or after recovery from pentobarbitone-induced (50 mg kg-1) anaesthesia. On the contrary, when mice were tested 6 h after a single exposure to the apparatus, pentobarbitone in either case failed to produce hyperactivity. The results demonstrate that mice recovering from barbiturate anaesthesia maintain susceptibility to the exteroceptive stimuli provided by a novel environment and knowledge of the environment acquired during past experience.

Anesthesia↗
PubMed1988

Tripelennamine enhances buprenorphine-, but not pentazocine-induced hyperactivity in mice.

The opioid agonist-antagonist pentazocine (1-30 mg/kg) and the partial agonist buprenorphine (0.05-0.25 mg/kg) were tested, alone or in combination with the histamine H1-receptor antagonist tripelennamine (1, 2.5, 5 or 10 mg/kg), on locomotor activity in mice of the CD-1 strain. When given alone, pentazocine produced slight and non-dose-related activity increments, while buprenorphine induced strong and dose-related locomotor stimulation. Tripelennamine slightly increased activity by itself and enhanced buprenorphine-, but not pentazocine-induced hyperactivity. The results are discussed in relation to the hypothesis that antihistaminic agents specifically interfere with locomotor effects of opioids.

Animals↗
PubMed1988

Enhancement of radial maze performances in CD1 mice after prenatal exposure to oxiracetam: possible role of sustained investigative responses developed during ontogeny.

A longitudinal study aimed at analyzing the behavioral effects of prenatal exposure to the nootropic compound oxiracetam was carried out in CD1 mice. Two groups of females were injected either with oxiracetam or saline from the beginning of pregnancy until parturition. Examination of pups from birth until the first month of age revealed no-influence of the treatment on litter size, body weights, sensory motor reflexes and motility. When placed in the open field at one month of age, mice born by mothers exposed to oxiracetam displayed more self grooming and spent less time in freezing than control mice. Prenatally treated mice were then found more interactive with their environment since the introduction of a novel object in the open field was followed by increased ambulation and higher sniffing object and rearing object scores. At three months of age, mice from both groups were tested in a radial six-arm maze task. Choice accuracy was significantly higher in prenatally treated mice which also tended to optimize their exploratory sequences by frequently running the maze in a clock-wise fashion. These results suggest that the better learning performances observed in the experimental group could be viewed as a consequence of an enhanced cognitive development based upon the higher rate of interactions with the environment shown by prenatally treated mice during ontogeny.

Animals↗
PubMed1988

Effect of naloxone on the locomotor stimulatory action of chlordiazepoxide in mice.

Locomotor activity was measured, during 60 min, in CD-1 mice receiving chlordiazepoxide (2.5 or 5 mg/kg) after a pretreatment with saline solution or naloxone (0.5, 1, 2.5 or 5 mg/kg). Both doses of chlordiazepoxide significantly increased locomotor activity in saline-pretreated mice. Naloxone prevented chlordiazepoxide-induced hyperactivity, at doses that did not themselves affect activity. This antagonistic action of naloxone indicates that opioid mechanisms are involved in the locomotor stimulatory effects exerted by chlordiazepoxide in mice.

Animals↗
PubMed1987

Antihistaminics enhance morphine-, but not amphetamine- and scopolamine-induced hyperactivity in mice.

Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine, amphetamine and scopolamine on locomotor activity in mice. All three antihistaminics, at some dosage levels, enhanced morphine-induced hyperactivity, but did not change or even reduce locomotor stimulation induced by amphetamine and scopolamine. The results suggest that H1-blocking agents may specifically interact, though not necessarily directly, with opiate mechanisms in producing behavioural effects.

Animals↗
PubMed1986

Facilitation of stimulatory effect of chlordiazepoxide-amphetamine combination by subacute administration of chlordiazepoxide in mice.

Spontaneous locomotor activity was tested in CD-1 mice receiving subacutely (for 4 days) chlordiazepoxide (10 mg/kg) and then treated with d-amphetamine (0.5 or 1 mg/kg) and various doses of chlordiazepoxide (2.5, 5 or 10 mg/kg) separately or in combination. Chlordiazepoxide pretreatment enhanced the stimulatory effect of the chlordiazepoxide-amphetamine combination.

Animals↗
PubMed1986

Avoidance facilitation in adult mice by prenatal administration of the nootropic drug oxiracetam.

CD-1 mice prenatally exposed to saline solution or to the nootropic drug oxiracetam (50 mg/kg during the whole pregnancy) were tested, when adults, for locomotor activity and for shuttle-box avoidance acquisition. Prenatal drug exposure produced long-lasting effects, evident in mature offspring. At the age of two months, mice prenatally exposed to oxiracetam showed a slight but significant reduction in locomotor activity. At the age of three months, these animals exhibited higher performances than control mice in avoidance acquisition.

Animals↗
PubMed1986

Enhancement of morphine-induced hyperactivity by antihistaminic drugs in mice.

Three histamine H1-receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine, were tested alone or in combination with morphine on locomotor activity in C57BL/6 mice. All three antihistaminics, at some dosage levels, slightly increased activity when given alone, but strongly enhanced morphine-induced hyperactivity. The results demonstrate that locomotor activity represents a useful test to evidence stimulatory effects of antihistaminic-opiate combinations.

Animals↗