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U Filibeck

Publications and source records attributed to U Filibeck.

15 recordsLinked to original sources
PubMed1992

Estimating the trend of the epidemic of drug use in Italy, 1985-89.

We used data from different sources to estimate the extent and the trend of the epidemic of drug use in Italy in the second half of the '80s. During the study period, the number of subjects attending drug dependency units increased from 13,905 to 61,689. Mortality and morbidity indicators showed an increase in both drug related deaths (mainly from overdose) and AIDS cases reported in injecting drug users, particularly among older subjects. However, the number of young adults detected as drug users at the army recruitment remained virtually stable from 1986 on. These findings suggest that both demand and availability of treatment increased through the years 1985-89, and that clinical consequences of drug use related behaviour have become an important public health priority.

Acquired Immunodeficiency Syndrome↗
PubMed1991

D1 and D2 receptor antagonists differently affect cocaine-induced locomotor hyperactivity in the mouse.

Pretreatment with small, per se ineffective doses of the selective D1 antagonist SCH 23390 inhibited hyperactivity induced by cocaine. On the other hand, the classic neuroleptic haloperidol and the selective D2 antagonist metoclopramide prevented the stimulatory effects of cocaine on locomotion only at hypokinetic doses, while the atypical neuroleptic (-)-sulpiride, a selective D2 antagonist, did not produce significant effects when administered at the hypokinetic dose of 12 mg/kg. Finally, at low doses (-)-sulpiride dose-dependently potentiated the locomotor-stimulating effects of cocaine, an effect that is not shared either with haloperidol or with metoclopramide. These results are discussed in terms of different roles of DA receptor subtypes in the modulation of the stimulant effects of cocaine on locomotion.

Animals↗
PubMed1988

Chronic cocaine enhances defensive behaviour in the laboratory mouse: involvement of D2 dopamine receptors.

C57BL/6 male mice injected with a challenge dose (20 mg/kg) of cocaine 72 h after the end of chronic intermittent treatment with the psychostimulant (two daily injections of 20 mg/kg for 10 days) exhibited a clear-cut increase in defensive upright and sideways postures and escape when confronted with a non-drugged conspecific. Treated mice spent 40% of time showing defensive acts over the 5-min testing session. Administration of the selective D2 receptor antagonist (-)-sulpiride (25 mg/kg) before the challenge dose of cocaine completely antagonized the increase in defensive behaviour, while the selective D1 receptor antagonist SCH 23390 (0.25-0.50 mg/kg) did not significantly affect defensive behavioural patterns. These results suggest the involvement of D2 receptors in cocaine-induced hyperdefensiveness. The hypothesis that alteration in D2 receptor functioning produced by chronic cocaine administration may produce hyperdefensiveness possibly due to altered perceptive processes is discussed.

Animals↗
PubMed1984

Naltrexone-reversible effects of flunitrazepam on locomotor activity and passive avoidance behaviour in mice.

Some behavioural effects of flunitrazepam were investigated in two sets of experiments in C57BL/6 mice. In the first set, flunitrazepam administration (0.025 or 0.05 mg/kg) enhanced the locomotor activity of mice. In the second set, memory impairments were observed following posttraining (immediately or 30 min, but not 60 min) treatment with the drug (0.05 mg/kg). All effects were antagonized by a per se ineffective dose of naltrexone (0.5 mg/kg for the activity, 0.1 mg/kg for the memory experiments), suggesting the involvement of opioid receptors. The results are discussed on the basis of recent evidence suggesting a link between benzodiazepine and opiate mechanisms of action.

Animals↗
PubMed1982

Behavioural data on dermorphins in mice.

Dermorphin, an opioid peptide occurring in amphibian skin, exerted a depressive effect on locomotor activity of C57B1/6 mice and an analgesic effect when injected intravenously. Intracerebroventricular injections of dermorphin enhanced locomotor activity and resulted in analgesia. A stimulating effect of intracerebroventricular administration on locomotor activity was also induced by shorter homologues of dermorphin and [D-Ala2, Leu5]enkephalinamide, while beta-endorphin produced a depression. It is suggested that dermorphin acts on central receptor populations activated by morphine and enkephalins.

Animals↗
PubMed1982

Lack of morphine-induced hyperactivity in C57BL/6 mice following striatal kainic acid lesions.

Bilateral injection of kainic acid (0.15 micrograms/0.3 microliters) into the striatum (caudatus/putamen) of C57BL/6 mice prevented stimulation of locomotor activity by morphine (20 mg/kg, i.p.). This effect was specific to morphine since mice with the same lesion did not show any impairment of amphetamine (2 mg/kg)-induced locomotor hyperactivity. Histological inspections showed neuron damage also in the nucleus accumbens, while hippocampus was not damaged by kainic acid. Moreover, mice with kainic acid lesions in the hippocampus were more stimulated by morphine, compared with the morphine-injected sham lesion group. The results, which suggest the existence of non-catecholaminergic mediations in the locomotor effects of morphine, are discussed in terms of opioid systems in the brain.

Amphetamine↗
PubMed1981

Cross-tolerance between D-amino acids and morphine in mice.

The effects of morphine administration on analgesia and running activity were studied in DBA/2 (DBA) and C57BL/6 (C57) mice respectively, injected with D-amino acids (D-AA) for 5 days. The results indicate a clear cross-tolerance between D-AA and morphine in DBA mice when analgesia is considered, while the stimulating effect of the opiate is not modified after D-AA pretreatment in the C57 strain.

Animals↗
PubMed1981

Differential effects of opiate agonists-antagonists on morphine-induced hyperexcitability and analgesia in mice.

The effects of two opiate agonists-antagonists, butorphanol (4.0 and 8.0 mg/kg) and buprenorphine (0.1 and 1.0 mg/kg), were assessed on locomotor activity and analgesia in DBA/2 and C57BL/6 mice. Different behavioral effects were evident in these strains, which might be characterized by different reactions to the effects of opiates and by differences in endorphin distributions and opiate receptor populations. In particular, buprenorphine acted as an agonist-antagonist to morphine in both strains while a dissociation of butorphanol effects was evident, depending on the strain considered. The clinical implications of these findings are discussed.

Analgesia↗
PubMed1981

Development of morphine-induced changes of activity in the mouse.

The development of spontaneous activity in response to morphine administration was studied at different postnatal ages in C57BL/6 mice. Morphine induced hyperactivity at all ages except in 3-week-old mice, in which a catatonic effect is evident. The results indicate that the neurophysiological and inhibitory systems responsible for the non-analgesic effects of morphine are not characterized by the same developmental pattern.

Aging↗
PubMed1980

Strain dependent effects of ketamine on locomotor activity and antinociception in mice.

The effects of ketamine (12.5, 25 and 50 mg/kg) on locomotor activity and response to nociceptive stimuli were investigated in the inbred strains of mice: BALB/c (BALB), C57BL/6 (C57) and DBA/2 (DBA). In the BALB and in the C57 mice ketamine exerted activity stimulating effects, which were already present at doses lower than those inducing antinociception. Locomotor depressent effects were evident in the DBA mice following the administration of doses higher than those necessary to induce analgesia. It is suggested that: (1) ketamine affects locomotor activity and response to painful stimuli through different mechanisms, (2) the brain regional and biochemical differences reported for the strains considered may account for their different responses to ketamine administtation.

Analgesics↗
PubMedDate not supplied

Cross-tolerance between amineptine, an atypical antidepressant and cocaine in mice.

The effects of amineptine and cocaine on locomotor activity were studied in two sets of experiments, by using C57BL/6 mice. In a first set, activity enhancements were evident following acute administration of both drugs. In addition to that the effects of amineptine were additive with those of cocaine. In a second set of experiments, mice developed tolerance to the stimulatory effects of both amineptine and cocaine, and a clear cross-tolerance effect was evident in mice chronically injected with these drugs. The results are discussed in terms of the involvement of dopaminergic mechanisms in the activity stimulating action of amineptine.

Animals↗
PubMedDate not supplied

Inhibition by clonidine of morphine-induced running fit but not analgesia in C57BL/6 mice.

Clonidine, 0.25 and 0.5 mg/kg, depressed significantly the running fit induced by 10 or 20 mg/kg of morphine in C57BL/6 mice, but did not affect morphine analgesia measured by the "hot plate" test. The results confirm the hypothesis that different mechanisms are involved in the two types of response to morphine, and the running fit response is mediated via a noradrenergic mechanism of action.

Analgesia↗