PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Locomotor activity”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

[Comparative study of the pharmacological properties of sultopride sulpiride and other antipsychotic drugs: influence of sultopride, sulpiride and other antipsychotic drugs on spontaneous locomotor activity and changes in locomotor activity induced by apomorphine and clonidine in mice].

To elucidate pharmacological properties of sultopride and sulpiride, their effects on spontaneous locomotor activity, apomorphine-induced hyper- and hypoactivity, and clonidine-induced hypoactivity in mice were examined by use of a photocell activity meter in comparison with the effects of other antipsychotic drugs. Sultopride did not affect spontaneous locomotor activity, whereas it potentiated apomorphine-induced hyperactivity at low doses and inhibited it at high doses. Sultopride also dose-dependently antagonized apomorphine-induced hypoactivity at limited doses. By contrast, sulpiride, in a wide range of doses, exhibited enhancement of apomorphine-induced hyperactivity and antagonization of apomorphine-induced hypoactivity. Furthermore, the activities of sulpiride were more potent than those of sultopride. Haloperidol and chlorpromazine inhibited spontaneous locomotor activity and apomorphine-induced hyperactivity and slightly antagonized apomorphine-induced hypoactivity. Pimozide increased spontaneous locomotor activity but inhibited it at high doses, while also potentiating apomorphine-induced hyperactivity at small doses and inhibiting it at large doses. Pimozide did not markedly affect apomorphine-induced hypoactivity. None of the drugs studied except for imipramine and yohimbine affected clonidine-induced hypoactivity. These results indicate that sultopride has somewhat different pharmacological properties from those of sulpiride and other antipsychotic drugs. These results also suggest that sultopride would have good therapeutic efficacy in schizophrenic disorders.

Amisulpride↗
PubMed1986

Decrease in d-methamphetamine sensitivity in mice due to ethanol: apparent inhibitory and stimulatory effects of ethanol on d-methamphetamine-induced locomotor activity.

The locomotor activity of mice was recorded after administration of d-methamphetamine-HCl (1.5, 2.5, 5.0 and 7.5 mg/kg body weight) and/or ethanol (0.8 and 1.6 g/kg body weight). Mice injected with lower doses of d-methamphetamine (1.5 or 2.5 mg/kg) showed a marked increase in locomotor activity, while in those with higher doses of d-methamphetamine (5.0 or 7.5 mg/kg), locomotor activity was not further enhanced, but slightly decreased. Administration of ethanol inhibited the stimulated locomotor activity caused by low doses of d-methamphetamine (1.5 or 2.5 mg/kg), while the stimulation of motility after higher doses of d-methamphetamine (5.0 or 7.5 mg/kg) was potentiated by administering ethanol. Although apparent inhibition and stimulation of d-methamphetamine-induced locomotor activity of mice due to ethanol was observed, it is suggested that mice administered ethanol showed the decreased sensitivity to d-methamphetamine by plotting total locomotor activity of mice against doses of d-methamphetamine administered. The half maximum effective dose of d-methamphetamine for locomotor activity was increased from 1.5 mg/kg to 3.0 mg/kg by concomitant administration of 1.6 g/kg ethanol.

Animals↗
PubMed1975

Influence of dopamine-like compounds on stereotypy and locomotor activity in atropinized rats.

The influence of atropine on stimulation of exploratory activity, locomotor activity and stereotypy in rats treated with compounds which stimulate central dopamine receptors (apomorphine, D-amphetamine, D-145 and piribedil) was studied. Atropine potentiated the action of these compounds in some experimental systems. The results are discussed from the point of view of an equilibrium between the dopaminergic and cholinergic systems in the central nervous system.

Animals↗
PubMed1991

Deprenyl (selegiline), a selective MAO-B inhibitor with active metabolites; effects on locomotor activity, dopaminergic neurotransmission and firing rate of nigral dopamine neurons.

Utilizing behavioral, biochemical and electrophysiological methods, central effects of the monoamine oxidase-B inhibitor deprenyl (selegiline) were analyzed. Administration of deprenyl (3-30 mg/kg, i.p.) caused a dose-dependent increase in the spontaneous locomotor activity. In the striatum, deprenyl (10 and 30 mg/kg) changed the dopa accumulation following 3-hydroxybenzylhydrazine hydrochloride in a biphasic manner. Deprenyl slightly decreased the firing rate of dopamine-containing neurons in substantia nigra, zona compacta. However, increases in locomotor activity and dopa accumulation induced by deprenyl were almost totally prevented by pretreatment with the microsomal liver enzyme inhibitor proadifen hydrochloride (50 mg/kg, i.p., 30 min), indicating that metabolites of the drug are of pharmacological significance for deprenyl's central actions. Furthermore, administration of l-methamphetamine, a major metabolite of deprenyl, affected spontaneous locomotor activity and striatal dopa formation and the firing rate of dopamine-containing neurons in the substantia nigra within the same magnitude as deprenyl itself when given in doses relevant to the formation of l-methamphetamine from deprenyl. However, unlike the effect of deprenyl, the l-methamphetamine-induced increase in locomotor activity and striatal dopa formation was not antagonized by pretreatment with proadifen hydrochloride. The data suggest that the stimulatory effect on locomotor activity and dopamine synthesis is not related to a monoamine oxidase-B blocking action of the drug or to a putative effect on DA reuptake, but rather to effects of metabolites of the drug (e.g., l-methamphetamine). It is proposed that metabolites of deprenyl should not be disregarded to account for the clinical benefits of the drug.

Animals↗
PubMedDate not supplied

Automating the measurement of locomotor activity.

General locomotor activity is assessed in many ways ranging from observer ratings to sophisticated computer-assisted electronic monitoring with the aim of determining the unconditioned and conditioned effects of various pharmacological compounds. A system was constructed utilizing 6 independent test chambers each equipped with 14 infrared emitters and detectors arranged in two tiers and controlled by a microcomputer. The effects of the stimulant, d-amphetamine and its antagonism by the tranquilizer, pimozide, on unconditioned and conditioned activity as assessed using this system were found to be almost identical to results obtained using observer rating techniques. Other data showed that activity assessed by the system was subject to habituation and that this learning interacted with the effects of some drugs. Activity as measured by the system showed dose and time effects of various stimulants assessed over a 6 hr test period. Finally, the breakdown of activity into counts on the upper and lower tier of beams resulted in the finding that these two components of behavior were differentially affected by stimulants. These results demonstrate the validity and reliability of automated systems for assessing locomotor activity and show their promise for gaining further insight into the elements of behavior that are affected by various drugs.

Animals↗
PubMed1991

Neither triazolam nor activity phase advance circadian locomotor activity in SCN-lesioned hamsters bearing fetal SCN transplants.

Both triazolam (Tz) and exercise can phase advance free-running locomotor activity rhythms in intact hamsters. Furthermore, Tz increases activity at the time of injection, and this appears to be the mechanism whereby Tz produces phase shifts. This study tested the phase-shifting effect of Tz in SCN-lesioned (SCN-X) hamsters that had regained circadian rhythms of locomotor activity after transplantation of fetal SCN into the third ventricle. The results indicate that in both groups, increases in locomotor activity are seen at the time of Tz injection, and most intact animals, but no grafted animals show a phase advance in response to Tz administration. Given that hamsters bearing SCN grafts have limited neural connections between the host brain and transplanted SCN tissue, the results suggest that a site outside the SCN, with afferents to these nuclei, mediates the phase-shifting effect of Tz and of exercise.

Animals↗
PubMed1988

The effect of chronic lithium administration and withdrawal on locomotor activity and apomorphine-induced locomotor stimulation in rats.

The effect of chronic lithium administration and withdrawal on locomotor activity and apomorphine-induced locomotor stimulation in rats was studied. Chronic lithium administration caused a decrease in locomotor activity, which might be due to a lithium-induced decrease of exploratory behaviour. Chronic lithium administration had no effect on apomorphine-induced locomotor stimulation. However, apomorphine-induced locomotor stimulation was increased two days after the withdrawal of lithium while no difference was found after four days, suggesting a transient increase in postsynaptic dopamine (DA) receptor sensitivity following lithium withdrawal.

Animals↗
PubMed1990

Effects of morphine, ethylketocyclazocine, N-allylnormetazocine and naloxone on locomotor activity in the rabbit.

Locomotor activity was studied in the rabbit following injections of morphine, ethylketocyclazocine and N-allylnormetazocine. All three drugs produced only depression of activity. The opioid antagonist naloxone antagonized the effects of both morphine and ethylketocyclazocine. Naloxone (0.1 mg/kg) did not antagonize the effects of N-allylnormetazocine. Naloxone alone depressed locomotor activity at doses above 0.3 mg/kg. This effect of naloxone was partially antagonized by 0.1 mg/kg ethylketocyclazocine, but not by 0.1 mg/kg morphine. The GABA agonist muscimol (0.1 and 1.0 mg/kg) also did not antagonize the effect of naloxone on locomotor activity. Finally, amphetamine did not produce a great deal of locomotor activation in the rabbit, which may indicate that increasing activity in the rabbit by drug intervention may be inherently difficult. These results indicate that the opioids have effects in the rabbit that are clearly different from those observed in rodents, where morphine and N-allylnormetazocine have been reported to produce locomotor activation, and naloxone typically has little effect. In addition, the effects of the opioids on locomotor activity were clearly distinguishable from their effects on learning in the rabbit. While morphine and ethylketocyclazocine were approximately equipotent in depressing locomotor activity, morphine is much less potent than ethylketocyclazocine in retarding acquisition of the classically conditioned nictitating membrane response in the rabbit.

Animals↗
PubMed1988

Differential effects on active avoidance performance and locomotor activity of two major enkephalin metabolites, tyr-gly-gly and des-tyr-[leu]enkephalin.

We examined the effects of two enkephalin metabolites, des-tyr-[leu]enkephalin and tyr-gly-gly, on one-way active avoidance conditioning in mice. These metabolites are products of the two major enkephalin hydrolyzing enzymes in plasma, aminopeptidase and angiotensin converting enzyme. Like [leu]enkephalin from which it may be formed, tyr-gly-gly impaired avoidance acquisition, and its dose-response function for this effect was U-shaped. Also like [leu]enkephalin, tyr-gly-gly did not alter locomotor activity. On the other hand, des-tyr-[leu]enkephalin, at the doses tested, was without effect on avoidance conditioning but produced decreased locomotion. These data suggest that the tyrosine end of the enkephalin molecule may be important for its effects on conditioning. Because of their low opioid potencies, it is unlikely that the behavioral actions of tyr-gly-gly and des-tyr-[leu]enkephalin are mediated through opioid receptors.

Animals↗
PubMed1991

Ventral pallidal microinjections of receptor-selective opioid agonists produce differential effects on circling and locomotor activity in rats.

Locomotor activity was investigated following microinjections of receptor-selective opioid agonists into the ventral pallidum (VP) of rats. In Expt. 1, male Long-Evans rats were treated with unilateral microinjections of the mu agonist [D-Ala2-MePhe4, Gly-ol5]-enkephalin (DAGO), the delta agonist [D-Pen2, D-Pen5]-enkephalin (DPDPE) or the kappa agonist U50,488H, and the rate and duration of circling behaviour were measured. DAGO (0.01, 0.1, 1.0 nmol) produced a dose-dependent increase in contralateral circling; pretreatment with 1.0 mg/kg naltrexone blocked the circling induced by the highest dose. The behavioral effect was largest when injections were targeted at the VP rather than structures dorsal to the VP. In contast to DAGO, intrapallidal DPDPE (0.01, 0.1, 1.0, 10.0 nmol) produced a slight increase in contralateral circling only at the highest dose and U50, 488H (0.01, 0.1, 1.0, 10.0 nmol) produced no effect. In Expt. 2, the effects of bilateral injections of DAGO, DPDPE and U50,488H were tested in photocell activity boxes. DAGO produced a dose-dependent increase in locomotor activity and this increase was decreased by 1.0 mg/kg naltrexone. A slight increase in activity was observed with the highest dose of DPDPE, and a slight decrease was observed with the highest dose of U50,488H. These findings confirm that opiate actions in the VP contribute to opiate-induced locomotion and suggest that mu and to some extent delta receptors are involved in this behavior.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

Apparent enhancement by SCH 23390 of apomorphine-induced locomotor activity in mice.

Effects of the dopamine (DA) D1 antagonist SCH 23390 and the DA D2 antagonist (-)-sulpiride on apomorphine-induced characteristic changes in spontaneous motor activity were investigated in mice using the system we have devised for automatically analyzing animal behaviors in mice. Apomorphine (3 mg/kg, SC) markedly increased parameters of spontaneous motor activity such as locomotor activity and rearing time. Apomorphine-induced increase in locomotor activity had peaks at 5-20 and 30-50 min after administration, and its trough was closely related to the marked increase in rearing time induced by this agonist. Apomorphine-induced locomotor activity accumulated over a 40-min period from 5 to 45 min after apomorphine injection, during which apomorphine-induced increase in rearing time peaked, was significantly increased by intraperitoneal administration of 0.03 and 0.1 but not 0.01 mg/kg SCH 23390. Apomorphine-induced increase in rearing time was dose-dependently depressed by this antagonist. In contrast, (-)-sulpiride (10-40 mg/kg, IP) decreased apomorphine-induced increases in rearing time and locomotor activity rather than enhancing the latter parameter. These data suggest that the apparent enhancement by SCH 23390 of apomorphine-induced locomotor activity is mediated through DA D1 receptors and does not always correlate with depression of apomorphine-induced rearing behavior in mice.

Animals↗
PubMed1986

Effects of serotonergic agonists and antagonists on the locomotor activity of neonatal rats.

The locomotor activity of neonatal rats was measured after treatment with serotonin agonists or antagonists. Treatment with the serotonin agonists 5-hydroxytryptophan or quipazine resulted in the elimination of the peak in activity which normally results from increases in activity from days 10 to 15 of life followed by decreases from days 15 to 20 of life. The drug-induced decreases in activity occurred at doses that did not alter locomotor activity after day 17, when most of the peak in activity had passed. The dose of 5 mg/kg of the serotonergic antagonist methysergide eliminated the peak in activity without changing locomotor activity after the peak had passed. The antagonists methiothepin and cinanserin only produced decreases in locomotor activity which did not appear to be related to the peak in activity. The serotonergic agonist data are compatible with the hypothesis that the development of the serotonin system contributed to the inhibition of locomotor activity. The methiothepin and cinanserin data neither confirm nor dispute the hypothesis, as their effects may have been either nonserotonergic or on serotonin receptors that were different than those acted on by the agonists.

5-Hydroxytryptophan↗
PubMed1992

Hypergravity and aging in Drosophila melanogaster. 6. Spontaneous locomotor activity.

The spontaneous locomotor activity (SLA) of Drosophila melanogaster flies kept at various gravity levels (1-5 g) was recorded in both longitudinal and cross-sectional experiments. No gravity level effect could be detected in the longitudinal one, probably because these flies were allowed (for technical reasons) to rest at 1 g for 15% of their life. By contrast, flies kept at 5 g in the cross-sectional experiment had lower SLA scores at middle and old age than both 1 and 3 g-kept flies. The results of this series of experiments on hypergravity (HG) effects on three forms of locomotor activity (climbing activity, patterns of movement and SLA) allow to conclude that aging is accelerated in HG, even if no longevity decrease could be detected in the 1-4 g range.

Aging↗
PubMed1991

Cocaine-induced locomotor activity in rats.

Rats were injected SC or IP with a dose of cocaine at 20 mg/kg twice daily or saline (2 ml/kg) for 15 consecutive doses. Horizontal (including ambulatory and repetitive activity) and ambulatory locomotor activities were assessed following the first (acute) and the 15th (chronic) injections. Total locomotor activity (area under curve, AUC) following the acute and the chronic administration of cocaine were comparable, regardless of the route of drug administration. However, the temporal patterns of activity were significantly different; the peak of locomotor activity occurred earlier (chronic vs. acute, 20 vs. 40 min after IP; 130 vs. 180 min after SC) following chronic cocaine administration. Furthermore, the peak activity was significantly higher (3-fold after IP and 50% after SC) in chronically than in acutely treated rats, providing evidence for sensitization. In contrast, activity in the late session (240-280 min after SC) was significantly lower following the chronic SC cocaine administration, providing evidence for desensitization. The absolute slope values of the ascending phase and the descending phase were significantly larger following chronic administration of cocaine than that following the acute dosing. The possibility of changes in locomotor activity with alteration of pharmacokinetics on chronic cocaine treatment is discussed.

Animals↗
PubMed1987

5-Hydroxytryptamine involvement in the locomotor activity suppressant effects of amphetamine in the mouse.

d-Amphetamine, in doses lower than required to increase motor activity, reduced mouse spontaneous locomotor activity when this was assessed using cages equipped with photocell units, using treadwheels, or the measurement of spontaneous climbing behaviour. Acute treatments with the serotonergic agonists quipazine and 5-hydroxy-DL-tryptophan also reduced wheel running activity, spontaneous locomotor activity assessed using photocell cages, and spontaneous climbing behaviour; fenfluramine caused a similar effect. Pretreatment with 5-hydroxy-DL-tryptophan enhanced the inhibitory effects of d-amphetamine. A 3-day treatment with fenfluramine, or lesions of the median raphe nucleus (but not the dorsal raphe nucleus) abolished the ability of d-amphetamine to reduce motor activity in the three test systems. It is concluded that low doses of d-amphetamine can reduce locomotor activity and that the effects may be mediated via an enhancement of the release of 5-hydroxytryptamine from the system arising in the median raphe nucleus.

Amphetamine↗
PubMed1989

Morphine-induced place conditioning is not confounded by drug-induced alterations in locomotor activity.

The influence of locomotor activity and environmental familiarity upon the reinforcing effects of morphine was examined in an unbiased place preference conditioning procedure. Groups of rats were trained to associate one distinctive environment with morphine and another with saline. One group was made tolerant to the locomotor activity effects of morphine by the SC administration of morphine (5.0 mg/kg/12 hr) for four days prior to conditioning. The other group received injections of saline. Administration of morphine, at doses which decreased locomotor activity, resulted in marked preferences for the drug-associated place in saline-treated rats. In contrast, chronic morphine treatment resulted in tolerance to the sedative effects of morphine and an abolition of the morphine-induced place preference. These results indicate that in the place conditioning procedure, measures of reinforcement are not confounded by drug-induced increases in activity.

Animals↗