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Biomedical subjects

M Sansone

Publications and source records attributed to M Sansone.

103 records · Page 6Linked to original sources

Stimulatory effect of chlordiazepoxide on locomotor activity in mice: importance of noradrenergic transmission.

Chlorodiazepoxide (CDP) produces stimulation of the locomotor activity of CD-1 and DBA/2 mice. This effect is strongly pronounced at the commencement of the testing session, and it is followed by a decline of the locomotor activity. The drugs impairing noradrenergic transmission: reserpine, clonidine and alpha-methyltyrosine, depressed or abolished the stimulatory effect of CDP; clonidine, in addition antagonized the subsequent decline of the locomotor activity in CDP-treated mice. Mice receiving reserpine subchronically (in the dose of 0.5 mg/kg daily for 3 days) displayed either motor depression or hypermotility. In approx. 50% of subchronically reserpinized mice CDP produced a strong hypermotility, lasting for at least 1 hr. It can be concluded that a noradrenergic mechanism is involved in the stimulatory effect of CDP on exploratory locomotor activity in mice, and that there exist two distinct subpopulations within the CD-1 strain, reacting differently to chronic reserpine treatment.

Animals↗

Opioid benzodiazepine tifluadom and drug-induced hyperactivity in mice: lack of benzodiazepine-like effects.

The opioid benzodiazepine, tifluadom, and the benzodiazepine tranquilizer, diazepam, were compared for their influence on morphine and scopolamine-induced locomotor stimulation in mice. Diazepam enhanced drug-induced hyperactivity, while tifluadom had no effect or reduced locomotor activity. The results demonstrate that tifluadom, a benzodiazepine compound possessing opiate-like analgesic properties, is devoid of either benzodiazepine or morphine-like effects in activity tests.

Animals↗

A toggle-floor box: the reliability of crossings in the evaluation of drug-induced locomotor changes in mice.

Various categories of the motor behavior were recorded using a video tape in mice subjected to a 10 min activity session in a toggle-floor box after an ip administration of saline solution, d-amphetamine (2 or 4 mg/kg), morphine (10 or 20 mg/kg) or scopolamine (0.5 or 1 mg/kg). While all the three drugs enhanced horizontal activity, in particular the crossing from one compartment to the other, rearing was inhibited, particularly by morphine. The results demonstrate that crossings, the behavioral category easily measurable automatically, represent a reliable index of the drug-induced hyperactivity.

Amphetamine↗

Antihistaminic-opioid combination: effect on locomotor activity in mice.

Various laboratory studies have been recently prompted by reports indicating abuse by heroin addicts of the narcotic agonist-antagonist pentazocine combined with the antihistaminic tripelennamine. For what concerns the effects on locomotor activity, it was demonstrated that three histamine H1 receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine enhance morphine-, but not amphetamine and scopolamine-induced hyperactivity in mice. These results suggested that antihistaminics may specifically interfere with locomotor effects of opioids. Such hypothesis was strengthened by further findings indicating enhancement by tripelennamine of the locomotor stimulation induced by buprenorphine, a drug possessing morphine-like properties.

Amphetamine↗

Effects of oxiracetam-scopolamine combinations on shuttle-box avoidance acquisition in mice.

The nootropic drug oxiracetam and the anticholinergic agent scopolamine were tested, alone or in combination, on shuttle-box avoidance acquisition and locomotor activity in mice of the CD-1 strain. Both drugs, given separately, slightly but significantly enhanced avoidance performance, but only scopolamine increased locomotor activity. Combinations of the 2 drugs, in some instances, enhanced avoidance performance more than drugs given separately, but the disinhibitory property of scopolamine makes it difficult to understand the role played by cholinergic mechanisms in these effects.

Animals↗

Tolerance to diazepam-induced avoidance depression in mice.

The disrupting action on avoidance responses, exerted by diazepam given during shuttle-box training (5 mg/kg before each session), was abolished by a pretreatment with the drug (5 mg/kg) for five days. Similarly, avoidance depression, produced by diazepam in trained mice, was prevented by a pretreatment with five daily doses and was attenuated by previous administration of three daily injections or even of a single dose of the drug. The results demonstrate that tolerance rapidly develops to diazepam-induced avoidance depression, as to other behavioral actions of benzodiazepines.

Animals↗

The effect of chronic administration of trazodone on the acquisition of avoidance behavior in mice.

An atypical antidepressant trazodone, given in doses of 5 or 10 mg/kg ip during the period of avoidance training (15 min before the beginning of each of 5 consecutive daily sessions) significantly depressed the rate of acquisition of the conditioned avoidance response. However, in mice pretreated with trazodone, 10 mg/kg daily for the preceding 14 consecutive days, the treatment with 10 mg/kg before each session did not impair the acquisition of the conditioned avoidance response, and the treatment with a dose of 5 mg/kg improved the acquisition over the control level. The data show that the pattern of action of trazodone on the acquisition of conditioned avoidance response is the same as that of other antidepressant agents, desipramine and mianserin, and indicate that chronically administered antidepressant agents do not impair learning.

Analysis of Variance↗

[Glomerulonephritis caused by a shunt: description of a case].

The authors report a case of shunt-nephritis due to bacteremia from Stafilococcus albus. Kidney biopsy, comprehensive of IF study allowed to assess the diagnosis of a disease from immunocomplexes. The Authors stress the importance of a close follow-up of patients who carry liquoral shunt for an early recognition of symptoms of glomerulopathy.

Cerebrospinal Fluid Shunts↗

Facilitation of avoidance behavior by chlordiazepoxide and chlordiazepoxide-amphetamine combination: effect on performance.

Chlordiazepoxide, 5 mg/kg, given at various stages of training invariably facilitated the shuttle box avoidance of CD-1 mice for a short period of time (100 trials); no after-effects were observed on the following daily session. Amphetamine, 1 mg/kg, usually did not facilitate significantly the responding, but its combination with chlordiazepoxide produced a stronger and more pronounced effect than that of chlordiazepoxide alone. In prolonged (600-trial) sessions the performance of mice declined in the second half of the session; this decline was temporarily reversed by chlordiazepoxide given alone or with amphetamine after the first 300 trials. The results indicate that the facilitation of shuttle-box avoidance behavior by chlordiazepoxide or chlordiazepoxide-amphetamine combination is due to the improvement of performance.

Amphetamine↗

Minaprine, but not oxiracetam, prevents desipramine-induced impairment of avoidance learning in mice.

The tricyclic antidepressant desipramine impaired shuttle-box avoidance acquisition in mice of the CD-1 strain. The nootropic drug oxiracetam was unable to prevent the desipramine-induced learning impairment, while a protective action was exerted by minaprine, a psychotropic agent regarded as an atypical antidepressant drug, possessing dopaminergic and related memory-enhancing properties. It seems likely that the dopaminergic action of minaprine played a determinant role in its avoidance improving effects in desipramine treated mice, because similar effects were produced by amphetamine. However, in contrast to amphetamine, minaprine did not enhance locomotor activity and did not show signs of general behavioral stimulation.

Animals↗

Shuttle-box avoidance behavior of mice treated with nifedipine in combination with nicotine or physostigmine.

Nicotine and physostigmine, given alone, slightly improved shuttle-box avoidance acquisition in mice. the dihydropyridine calcium channel inhibitor nifedipine, ineffective alone, enhanced the avoidance facilitating action of nicotine, but prevented the slight improving action of physostigmine. The results confirm that calcium channel blockers can interfere with the effects of centrally acting drugs and may augment the facilitation of learning induced by some of them. However, a comparison of the effects of nifedipine with those of the noncalcium antagonist vasodilator hydralazine suggests that hypotensive action of calcium channel blockers may interfere with the behavioral action related to specific neuronal changes due to calcium channel blockade. This may be particularly important in cases in which hypotensive action is exerted by the agent used in combination with the calcium channel blocker.

Analysis of Variance↗

Enhancement by nifedipine of cholinergic-induced depression of locomotor activity in mice.

The dihydropyridine calcium channel blocker nifedipine did not affect spontaneous locomotor activity in mice when given alone but enhanced the depressant effects of the muscarinic receptor agonist oxotremorine and of the acetylcholinesterase inhibitor physostigmine. Such a behavioral depression might be due to neuronal changes induced by central calcium channel blockade combined with cholinergic activation. However, an involvement of hemodynamic factors, related to peripheral vasodilatation, cannot be excluded as locomotor depressant effects were also exerted by combinations of the two cholinomimetic agents with hydralazine, a non-calcium antagonist vasodilator.

Animals↗

Locomotor activity pattern induced by diazepam in control and caffeine-treated mice.

The effect of diazepam on locomotor activity was tested by measuring the number of crossings between two compartments of a toggle-floor box, in control mice (water drinking) and in mice receiving caffeine solution (0.5 g/I) instead of drinking water. In control mice, diazepam did not produce any significant change in total activity measured on the whole 60-min test, but animals showed phases of increased activity broken by periods of immobility. After chronic ingestion (18 days) of caffeine, doses of 0.5, 1 and 2 mg/kg ip diazepam significantly increased total locomotor activity. Caffeine slightly reduced diazepam-induced immobility and increased the frequency of crossings in active periods. Taken together, these two effects may explain the significant increase in total activity induced by diazepam in caffeine-treated mice. Mixed stimulatory-depressant action was also produced by 3 mg/kg diazepam, a dose that slightly decreased the total activity.

Animals↗