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Results for “Locomotor activity”

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At least 19 recordsLinked to original sources
PubMed1979

Age-dependent effects of 6-hydroxydopamine on locomotor activity in the rat.

This experiment examined the effects on locomotor activity of intraventricular 6-hydroxydopamine (6-OHDA) administered to developing and adult rats. 6-OHDA was administered subsequent to pargyline treatment at 3 and 6 days of age; or 6-OHDA was administered subsequent to desmethylimipramine (DMI) treatment (6-OHDA/DMI) at 3 and 6 days of age, 11 and 14 days of age, 20 and 23 days of age, or 46 and 48 days of age. Locomotor activity of vehicle-treated rats assessed in stabilimeter cages peaked between 14 and 16 days of age and subsequently declined to levels characteristic of the adult. Treatment with pargyline and 6-OHDA at 3 days of age, or 6-OHDA/DMI at 3 and 6 or 11 and 14 days of age, did not alter the early rise in locomotor activity but prevented the decline in activity normally seen during the third and fourth weeks of life. When tested as adults, locomotor activity was greater in rats that had been treated with 6-OHDA/DMI at 3 and 6 and at 11 and 14 days of age than in those that had been treated at 20 and 23 days of age. Treatment with 6-OHDA/DMI at 46 and 48 days of age was without significant effect on locomotor activity. 6-OHDA (with pargyline pretreatment) produced large decreases in NE content in telencephalon and diencephalon and in dopamine (DA) content in striatum. 6-OHDA-DMI also produced large decreases in DA content in striatum and, in some of the treatment groups, only small decreases in norepinephrine (NE) content in telencephalon, diencephalon, and brain stem. These data suggest that the maturation of neuronal systems utilizing dopamine as a neurotransmitter is essential for the suppression of locomotor activity normally seen during development. The data further suggest that dopamine depletion per se does not lead to increased locomotor activity, but rather it is the destruction of dopamine-containing fibers prior to the normal period of locomotor suppression that increases locomotor activity.

Age Factors↗
PubMed1979

[Studies on the change of spontaneous locomotor activities in rats due to forced exercise (author's transl)].

The authors have devised an apparatus for monitoring the spontaneous locomotor activity of rats, with which the patterns of locomotor activity under the condition of light-dark cycle (light period: twelve hours from 6 a.m., dark period: the other half of the day) were analysed. In addition, changes in locomotor activities due to forced exercise (swimming) were recorded. The results obtained were as follows: 1. The patterns of locomotor activities in rats recorded by the monitor showed the same patterns as reported already by other researchers. The authors believe that this new apparatus can be used practically as a locomotor activity monitor. 2. Due to exhaustive exercise by swimming, changes of the ultradian rhythm in rats were observed. 3. By loading of swimming, locomotor activities in rats decreased significantly, especially in the dark period. These results suggest that this newly devised apparatus is useful as a locomotor activity monitor, and that the fatigue in rats caused by physical load can be shown as the change in locomotor activities.

Animals↗
PubMed1978

Simultaneous determination of circadian rhythms of locomotor activity and body temperature in the rat.

Stimultaneous determination of the circadian rhythms of locomotor activity and body temperature was carried out in the rat. Deep body temperature was monitored continuously using a telemetric device. The circadian rhythm of locomotor activity was characterized by clustering of several bursts of activity during the dark period. The circadian rhythm of body temperature was also characterized by bursts of small fluctuations which were well correlated with those of locomotor activity. Correlation between the two functions was such that the regression line expressing body temperature as a function of locomotor activity had approximately the same slope for dark and light periods, but a body temperature for a given amount of locomotor activity was significantly higher during the dark period than during the light one. After a prolonged exposure to constant light, the circadian rhythm disappeared in both functions. Both showed bursts of fluctuations which were correlated with each other. These results indicate that the bursts of body temperature increment were dependent on those of the locomotor activity. However, manifestation of the circadian rhythm per se of body temperature could not be explained as resulting exclusively from the circadian fluctuation of locomotor activity.

Animals↗
PubMed1976

Effects of scopolamine and d-amphetamine on locomotor activity before and after shock: a diallel analysis in mice.

The effect of shock on locomotor activity was evaluated in three strains of mice (A, DBA/2 and C57BL/6) after treatment with scopolamine (1.0 mg/kg) and d-amphetamine (10.0 mg/kh). The effectiveness of either drug in incrasing locomotor activity was strain dependent. Both drugs eliminated behavioral suppression induced by shock, and in A and DBA/2 mice shock augmented the locomotor stimulation induced by d-amphetamine. In another experiment the behavior of the 6 F1 hybrids was examined in relation to the parent strains. It was observed that locomotor activity in the F1's could resemble that seen in one parent in the saline condition, but the other parent after treatment with d-amphetamine. Similarly, the F1 behavior in the amphetamine condition was not predictive of the behavior seen after shock plus amphetamine. The results suggest that general activity, locomotor activity after amphetamine treatment, and responsiveness following shock in amphetamine-treated mice are mediated by different genetic mechanisms.

Animals↗
PubMed1978

Reversal of adenine-induced depression of mouse locomotor activity by amphetamine.

Adenine (200 mg/kg) was found to depress locomotor activity in mice. Dl-, and d-amphetamine reversed the depression of locomotor activity produced by adenine while l-amphetamine was found to be incapable of reversing the adenine-induced depression. The stimulation of mouse locomotor activity caused by dl- and d-amphetamine in mice treated with adenine was less than that caused by equal dosage of these agents in mice not treated with adenine. Mice treated with adenine showed marked depletion of brain norepinephrine, dopamine and serotonin, irrespective of whether or not they had been treated with d- or l-amphetamine, and whether or not these agents were capable of reversing adenine-induced depression of locomotor activity.

Adenine↗
PubMed1978

Effect of clonidine, amphetamine, and their combinations on the locomotor activity of CD-1 and C57BL/6 mice.

Clonidine inhibited the exploratory motor activity of C57BL/6 mice non-habituated to the testing conditions. In CD-1 mice clonidine did not depress exploratory activity but did elevate the basal locomotor activity of animals both non-habituated and habituated to testing conditions. Amphetamine increased the locomotor activity of many C57BL/6 mice and conversely inhibited the locomotion of many CD-1 mice. In both strains, amphetamine in doses up to 2 mg/kg was unable to alter effects produced by clonidine. Results suggest that the locomotor activity of C57BL/6 mice is more sensitive than that of CD-1 mice to drugs affecting the central noradrenergic system.

Amphetamine↗
PubMed1979

Spontaneous locomotor activity and food and water intake in rats with medial amygdala lesions.

Locomotor activity was studied with the method of electromagnetic activity meters, before and after operation in rats bilaterally lesioned in medial amygdala, and in a sham-operated control. Two activity tests were performed daily. In the first test spontaneous activity was recorded for a 30 min period without access to food or water. The second test measured 12 h of nocturnal activity with full access to food and water. Bilateral destruction of the medial amygdala resulted in an increase of locomotor activity in the 30 min test and a decrease in locomotor activity in the 12 h test. Postoperative decrease in food and water intake and body weight were only transient. These results point to a participation of the medial amygdala in the complex mechanism of locomotor activity and alimentary motivation.

Amygdala↗
PubMedDate not supplied

Central action of narcotic analgesics. II. Locomotor activity and narcotic analgesics.

The effect of morphine, codeine, fentanyl and pentazocine on locomotor activity of rats and mice and open-field performance of rats were tested. All the analgesics tested produced a depressive action in the rat. In mice a depressive action was produced by pentazocine and codeine. Fentanyl increased the exploratory and basal locomotor activity of mice. Morphine increased the exploratory activity, but, given at doses of 2.5 and 10 mg/kg decreased the basal locomotor activity. The increase of locomotor activity in mice by morphine and fentanyl is caused by an indirect stimulation of catecholamine receptors.

Analgesics, Opioid↗
PubMedDate not supplied

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↗
PubMed1979

Schedule-induced locomotor activity in humans.

In two experiments, humans received tokens either on a fixed-interval schedule for plunger pulling or various response-nondependent fixed-time schedules ranging from 16 to 140 seconds. Locomotor activity such as walking, shifting weight, or pacing was recorded in quarters of the interreinforcement interval to examine the induced characteristics of that behavior in humans. While performance was variable, several characteristics were present that have counterparts in experiments with nonhumans during periodic schedules of food reinforcement: (a) first quarter rates, and sometimes overall rates, of locomotor activity were greater during intervals that terminated in a visual stimulus and token delivery than those without: (b) overall rates of locomotor activity were greater during fixed-time 16-second schedules than during fixed-time 80- or 140-second schedules; (c) rates of locomotor activity decreased during the interreinforcement intervals; (d) locomotor activity was induced by response-dependent and response-nondependent token delivery. These results showed that the rate and temporal pattern of locomotor activity can be schedule-induced in humans.

Adolescent↗
PubMed1976

Age, sex and genotype effects on stimulus exploration and locomotor activity in young mice.

Age and sex effects on stimulus exploration and locomotor activity were investigated in three genetic stocks of mice. Three measures of exploratory behavior and one measure of locomotor activity were recorded in an arena testing situation. The results showed that measures requiring locomotor activity are more affected by differences in age and sex than measures of stimulus exploration. The results are discussed in terms of the previously established genetic models of stimulus exploration and activity.

Age Factors↗
PubMed1979

Behavioral rating scales for assessing phencyclidine-induced locomotor activity, stereotyped behavior and ataxia in rats.

Behavioral rating scales were developed for quantification of phencyclidine (PCP)-induced locomotor activity, stereotyped behavior and ataxia in rats. The dose-response relationship for PCP-induced locomotor activity was found to be an inverted U-shaped function over the first 25 min after injection while over the last 30 min of the experiment the function was highly linear. A linear dose-response relationship was found for ratings of stereotyped behavior and ataxia throughout the 90 min period of observation. The ratings of these two behaviors were found to be closely parallel. The effects of PCP on locomotor activity were found to be greatest during those intervals when stereotyped behavior and ataxia were at moderate levels. Ratings of locomotor activity may be confounded by ataxia when PCP is administered alone or in combination with other drugs.

Animals↗
PubMed1976

Effects of heroin, alone or in combination with other drugs, on the locomotor activity in two inbred strains of mice.

The locomotor activity of C57Bl/6J and DBA/2J mice was studied, under the influences of heroin, amphetamine, strychnine, or ethanol, and of combinations of the opiate with each one of the other drugs. Heroin treatment was followed by the typical "running fit" in the C57 mice, while the DBA strain was unaffected. Amphetamine enhanced the activity in the C57 strain only. The combination of heroin with amphetamine or ethanol increased the locomotor activity only in the DBA strain, while heroin + strychnine exerted a clear stimulating effect on the activity of the C57 mice. The strychnine + heroin mixture was more toxic than heroin alone when the lethal doses (LD50) were determined in the 2 strains.

Amphetamine↗
PubMed1976

The role of locomotion in conditioning methylphenidate-induced locomotor activity.

This experiment determined whether overt performance of the entire response (actual running) was necessary for the conditioning of methylphenidate-induced locomotor activity (wheel-running) in guinea pigs. Four guinea pigs were given daily injections of 2.5 mg/kg methylphenidate and were allowed to run in activity wheels; 4 other guinea pigs were given methylphenidate and were placed in locked activity wheels; a third group of 4 guinea pigs were administered saline and allowed to locomote; a fourth group of 4 guinea pigs received saline injections and were placed in locked activity wheels. After 12 days of injection, all animals were given saline injections on the 9 subsequent days and allowed to run freely in the wheels. The 2 groups which had received methylphenidate showed more locomotor activity than the saline injected animals but were not distinguishable from each other on the basis of prior opportunity to engage in locomotor activity. These results were interpreted to indicate that (a) increased methylphenidate-induced locomotor activity may be conditioned with repeated administration of the drug, and (b) actual running is not essential for the conditioning of drug-induced wheel-running.

Adaptation, Psychological↗
PubMed1979

Effects of parachlorophenylalanine and 5, 6-dihydroxytryptamine on the free-running rhythms of locomotor activity and plasma corticosterone in the rat exposed to continuous light.

Parachlorophenylalanine (PCPA) and 5,6-dihydroxytryptamine (5,6-DHT), depletors of brain serotonin, were administered to the rat and circadian rhythms of locomotor activity and plasma corticosterone were determined simultaneously in individual rats in light-dark cycles (LD) and in 200 lux continuous light (LL). Free-running periods and acrophases on the 12th day in LL (LL12) were calculated by a least squares spectrum method. In PCPA-treated rats which showed 70% depletion of brain serotonin, circadian rhythms of locomotor activity in LL and of plasma corticosterone and ACTH in LD disappeared for several days after the drug injection. Circadian rhythms of locomotor activity reappeared after the LL7 day and free-ran with a phase shift. Free-running periods of these rats did not differ significantly from that of control rats. However, the acrophase of PCPA-treated group on the LL11 day was 5 h advanced as compared to that of control. Circadian rhythm of plasma corticosterone in the PCPA-treated rats was detected on the LL12 day but their peak times were distributed around 24:00 h instead 08:00 h observed rats. The 5,6-DHT-treated rats which showed only 40% depletion of brain serotonin exhibited normal free-running rhythms in both locomotor activity and plasma corticosterone in LL and no difference in the acrophases of these functions on the LL12 day as compared to controls. These results suggest that PCPA affects the circadian clock (or clocks) itself in such a way that it blocks the clock to free-run or at least it effectively shortens the free-running periods of locomotor activity and plasma corticosterone in the rat.

5,6-Dihydroxytryptamine↗
PubMed1978

The involvement of catecholamine in scopolamine-induced locomotor activation and rotational behaviour in mice.

Scopolamine-induced locomotor activation was studied in comparison with the responses to apomorphine and methamphetamine in mice. The responses to scopolamine and methamphetamine were markedly depressed by the pretreatment with the catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine, while the activation response to apomorphine was not affected. p-Chlorophenylalanine did not affect the response to scopolamine. Phenoxybenzamine reduced the responses to scopolamine and methamphetamine, but did not affect the apomorphine response. Propranolol did not affect the responses to the three agonists, scopolamine, apomorphine and methamphetamine. Antipsychotic drugs haloperidol and pimozide reduced the responses to the three agonists. Haloperidol was especially effective in this regard. These results suggest the involvement of catecholamine in the locomotor activation produced by scopolamine. In the rotational behaviour model which is sensitive to dopamine receptor stimulating agents, effects of the three agonists were studied. Scopolamine produced the ipsilateral rotation in mice with unilateral striatal 6-hydroxydopamine-induced lesions. Methamphetamine induced the ipsilateral rotation, while apomorphine produced the contralateral rotation. The rotations induced by three agaonists were suppressed by pimozide. The results indicate the participation of dopamine in the scopolamine-induced rotational behaviour in mice.

Animals↗
PubMed1978

Tolerance development to the biphasic effects of morphine on locomotor activity and brain acetylcholine in the rat.

The development of tolerance to the depressant and stimulant actions of morphine on locomotor activity and brain acetylcholine (ACh) utilization (indirect turnover) was investigated in the rat. When administered to nontolerant rats, 1.0 mg/ kg s.c. of morphine produced an increase in locomotor activity and a concomitant increase in ACh utilization. Larger doses produced biphasic effects on locomotor activity, but only 10 mg/kg s.c. resulted in both an initial decrease and subsequent increase in ACh utilization in whole rat brain. The depressant and stimulant actions of morphine on both endpoints were antagonized by 1.0 mg/kg i.p. of naloxone administered 30 min before the maximum effect. Tolerance to morphine was produced by t.i.d. injections of increasing doses. Rapid tolerance developed to the locomotor depressant actions of morphine and to the decrease in brain ACh utilization. Tolerance to the depressant effects resulted in an enhanced stimulant action. Tolerance also developed to the stimulant actions of morphine but only when large doses of drug were administered daily. Biphasic effects of 10 mg/kg of morphine on brain ACh utilization were also observed in the hippocampus, thalamus and hypothalamus. Only a decrease in ACh utilization was observed in the caudate nucleus. Tolerance developed to the decreases and increases in ACh utilization in these discrete brain regions. This study demonstrates that tolerance development to the depressant and stimulant actions of morphine is complex and involves different dose and time schedules. It is not possible therefore to study tolerance to the actions or morphine without specifying the precise endpoint studied and the tolerance schedule utilized.

Acetylcholine↗