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At least 865 records · Page 48Linked to original sources
PubMed1986

Lack of the effect of ketamine on some dopaminergic behaviors in rats.

The effects of ketamine on some experimental models for detecting dopaminergic activity were studied in rats. Small doses of ketamine (0.3 and 0.5 mg/kg, ip) induced yawning behavior while higher doses (15 and 30 mg/kg, ip) inhibited both apomorphine- and amphetamine-induced stereotyped behaviors. Ketamine (up to 60 mg/kg, ip) per se failed to elicit typical stereotype or catalepsy similar to that induced by dopamine agonists or antagonists, respectively. Ketamine may have acted as an agonist on dopaminergic autoreceptors. These results do not support the view that the behavioral effects of ketamine are mediated by purely dopaminergic mechanisms.

Animals↗
PubMed1976

Climbing behavior induced by apomorphine in mice: a simple test for the study of dopamine receptors in striatum.

Mice treated with low doses of apomorphine tend to adopt a vertical position along the walls of their cage. Optimal conditions have been defined to obtain a reliable dose-response relationship. This peculiar behavior appears to be elicited by stimulation of dopamine receptors in the striatum: it is suppressed after coagulation of this structure while it is facilitated when these receptors are made hypersensitive by previous treatments with 6-hydroxy-dopamine or haloperidol; on the other hand, it is not modified by coagulation of the nucleus accumbens. The relative efficacy of various agonists and antagonists of dopamine receptors have been determined on this test. It appears that this stereotyped behavior might represent a convenient mean to assess the stimulation of striatal dopamine receptors in mice.

Animals↗
PubMed1995

Effects of chronic treatments with SM-9018, a potential atypical neuroleptic, on behavioral dopaminergic and serotonergic sensitivities in rats.

1. Changes in behavioral dopaminergic and serotonergic sensitivities were studied in rats after withdrawal of the chronic treatments with SM-9018 (0.1 mg/kg/day), a potential atypical neuroleptic, and with haloperidol (0.3 mg/kg/day) using continuous infusion pumps. 2. Administration of SM-9018 inhibited the rat locomotor activities to an extent similar to that of haloperidol during the course of the 2 weeks treatment. 3. The incidence of the apomorphine-induced stereotyped behaviors (e.g., sniffing, chewing, licking and biting) was negligibly affected by SM-9018 treatment, but was markedly enhanced by haloperidol treatment. 4. The incidence of the 5-hydroxytryptophan-induced wet dog shakes and 8-hydroxy-2-(di-n-propyl-amino)tetralin-induced flat body posture was unaffected by either treatment with SM-9018 or haloperidol. 5. These findings suggest that SM-9018 is weaker than haloperidol in inducing the behavioral dopaminergic hypersensitivity after its chronic treatment and has a lower propensity to cause tardive dyskinesia.

5-Hydroxytryptophan↗
PubMed1989

Amphetamine stereotypy in cats and neurotransmitter interactions in the caudate nucleus. I. Effects of intracaudate injections of haloperidol, GABA and bicuculline.

Intracaudate (into the rostrodorsal part of the caudate nucleus) injection of haloperidol in free moving cats did not modify spontaneous or d-amphetamine-induced stereotyped behavior, while administered intraperitoneally, haloperidol blocked the stereotypy. These results, in accordance with some views, suggest that in this region of the caudate nucleus, the dopamine inhibitory receptors prevail over the excitatory ones. The effects of intracaudate bicuculline (decrease in the number of all stereotyped movements, increase in the number of ipsilateral amphetamine-induced or spontaneous head movements over the contralateral ones) were more pronounced than those of intracaudate GABA (increase only in the number of nonfocused lickings). The present results support the view that interactions between dopamine and GABA occur in the caudate nucleus in cats during amphetamine stereotypy.

Amphetamine↗
PubMed1990

Effects of a Palicourea marcgravii leaf extract on some dopamine-related behaviors of rats.

The effects of a Palicourea marcgravii leaf extract on some dopamine-related behaviors were studied in rats. The extract given subcutaneously decreased both spontaneous locomotion and rearing frequencies of rats observed in open-field studies and increased their periods of immobility. The extract was also able to produce a rightward displacement of the apomorphine dose-response curve for stereotyped behavior and decrease the maximum response possible. Although the extract (1.87 g/kg subcutaneously) was unable to produce true catalepsy by itself, it potentiated that induced by haloperidol. These results with the extract can be interpreted to be due to a direct blocking action for the extract on a mesostriatal dopamine receptor or to an indirect effect on dopamine pathways through central cholinergic activation.

Animals↗
PubMedDate not supplied

Behavioral effects of dibutyryl cyclic 3'5'AMP and biogenic amines in rats.

White male Wistar rats were injected intraventricularly with 200 mug of dibutyryl cyclic 3'5'AMP (DAMP. 30 min later part of animals was injected intraventricularly with 10 mug of dopamine (DA), 10 mug of 5-hydroxytryptamine (5-HT) or 50 mug of acetylcholine (Ach). Immediately after injection of the amines the time of walking, convulsions, immobility and number of jumps during 10 min periods of observation was measured. DAMP induced excitation of animals expressed by convulsions, jumping and short period of immobility. All studied biogenic amines inhibited convulsions and caused periodically stereotypical behavior. 5-HT and Ach increased the time of immobility in animals injected with DAMP. DA increased the number of jumping. These results indicate the interaction between DAMP and DA, 5-HT and Ach on behavioral phenomena in rats.

Acetylcholine↗
PubMed1993

The effect of peripheral inositol injection on rat motor activity models of depression.

Myo-inositol is an important precursor in cellular second-messenger synthesis. It has been reported to be reduced in the cerebrospinal fluid of depressed patients and to reverse a specific effect of Li on rat behavior when given intracerebroventricularly (i.c.v.). However, myo-inositol enters the brain poorly when given peripherally, and its effects on normal rat brain have not been well studied. A series of experiments examined the effect of intraperitoneal inositol in high doses on locomotor activity, on amphetamine-induced hyperactivity, on apomorphine-induced stereotyped behavior, and on pilocarpine-induced behaviors in rats. In addition, the behavioral effect of i.c.v. inositol was compared to that of a control stereoisomer in untreated and lithium-treated rats. Few effects of peripheral myo-inositol were found in these models. However, peripheral inositol in high doses given to rats exhibiting Li-pilocarpine seizures showed that i.p. inositol could prevent these behaviors, confirming that peripheral inositol may have antidepressant potential in appropriate models.

Amphetamine↗
PubMedDate not supplied

Glucocorticoids modulate behavioral effects induced by dopaminergic agonists in rats.

Studies showing the presence of glucocorticoids, and their binding sites in the central nervous system indicate that these hormones may affect central neurotransmission. Both, dopaminergic brain system and glucocorticoids are considered to be involved in certain psychopathological conditions in humans, including depression, addiction or schizophrenia. The present study aimed to investigate the influence of glucocorticoids on dopamine agonists-induced stereotyped behavior and locomotor hyperactivity in rats. The results of the experiment demonstrate that prior to administration of prednisolone (4, 6, 10 or 20 mg/kg) or dexamethasone (4 or 8 mg/kg) intensified and prolonged the stereotypy induced by apomorphine (1 mg/kg sc) or amphetamine (2 mg/kg ip). The effect of dexamethasone was more potent. Amphetamine (0.4 mg/kg)- or amantadine (50 mg/kg)-induced locomotor hyperactivity was significantly reduced in rats pretreated with dexamethasone at a dose of 8 mg/kg or 4 mg/kg. Our observations suggest that exogenous glucocorticoids may enhance the activity of the dopaminergic agonists in the striatum but reduce it in the mesolimbic system of rats.

Animals↗
PubMed1997

Paradoxical behavioral response to apomorphine in tenascin-gene knockout mouse.

Tenascin is a large extracellular matrix glycoprotein which is highly expressed in the developing nervous system. To examine the role of tenascin in vivo, we have produced mice in which the tenascin-gene is inactivated. These animals did not easily habituate to unfamiliar circumstances and displayed hyperlocomotion. A dopamine receptor agonist, apomorphine, reduced this hyperlocomotion dose dependently, but this phenomenon was not due to the appearance of apomorphine-induced stereotypic behavior, suggesting that tenascin-gene mutant mice have a paradoxical behavioral response to apomorphine compared to wild-type mice.

Animals↗
PubMed1992

Organization of the stretch response to milk in the rat fetus.

Intraoral infusion of milk reliably elicits a stretch response in the rat fetus. The fetal stretch response appears isomorphic to the stereotypic behavior exhibited postnatally by suckling rat pups during milk ejection. Using a procedure that permits direct fetal observation, milk infusions were delivered to rat fetuses on Day 20 or 21 of gestation. Infusion of milk promoted systematic changes in fetal behavior that culminated in expression of the stretch response nearly 3 min later. Interruption of this behavioral sequence prevented stretching, suggesting that a period of behavioral reorganization after milk infusion is necessary but not sufficient for the stretch response to occur. The behavioral sequence initiated by the fetal rat's first exposure to milk is remarkably similar to the behavior exhibited by experienced infant rats at the nipple.

Animals↗
PubMed1983

Effects of electroconvulsive shock on monoaminergic systems in the rat brain. Thesis.

The effects of single or repeated electroconvulsive shock (ECS) (once daily for 7 days) on rat behavior and on the level, utilization and uptake of biogenic amines in rat brain were studied between one and ten days after the last ECS. It has been found that a single ECS caused catalepsy and analgesia, depressed locomotor activity and locomotor hypermotility produced by amphetamine and nomifensine (but not by apomorphine) and decreased the frequency of head twitch response evoked by LiCl. Repeated ECS also induced catalepsy and analgesia but enhanced both the spontaneous locomotor activity and amphetamine, nomifensine and apomorphine-induced hypermotility, and increased the frequency of head twitch response produced by LiCl, 5-HTP and 5-methoksytryptamine. Single and repeated ECS did not change exploratory motility or stereotyped behavior induced by apomorphine, but enhanced haloperidol-induced catalepsy and altered dopamine and serotonin levels in the rat brain. The utilization of NA and DA was not changed by repeated ECS, whereas the uptake of these amines was slightly reduced. The present results provide evidence that a single ECS depresses but repeated ECS augments some behavioral responses to dopaminergic and serotonergic agonists. The possible biochemical mechanisms involved in these effects of ECS are discussed.

Animals↗
PubMed1998

A novel pentadecapeptide, BPC 157, blocks the stereotypy produced acutely by amphetamine and the development of haloperidol-induced supersensitivity to amphetamine.

BACKGROUND: A novel gastric pentadecapeptide, BPC 157, has been shown to attenuate different lesions (i.e., gastrointestinal tract, liver, pancreas, somatosensory neurons). This suggests an interaction with the dopamine system. When used alone, BPC 157 does not affect gross behavior or induce stereotypy. METHODS: We first investigated the effect of pentadecapeptide BPC 157 on stereotypy and acoustic startle response in rats, given as either a prophylactic (10 micrograms/kg i.p.) or therapeutic (10 ng/kg i.p.) regimen, with the dopamine indirect agonist amphetamine (10 mg/kg i.p.). RESULTS: There was a marked attenuation of stereotypic behavior and acoustic startle response. When the medication was given at the time of maximum amphetamine-induced excitability, there was a reversal of this behavior. A further focus was on the effect of this pentadecapeptide on increased climbing behavior in mice pretreated with the dopamine antagonist haloperidol (5.0 mg/kg i.p.), and subsequently treated with amphetamine (20 mg/kg i.p. challenge 1, 2, 4, and 10 days after haloperidol pretreatment). This protocol is usually used for the study of behavioral supersensitivity to the amphetamine stimulating effect. CONCLUSIONS: An almost complete reversal was noted when pentadecapeptide was coadministered with haloperidol. Together, these data provide compelling evidence for the interaction of pentadecapeptide BPC 157 with the dopamine system.

Amino Acid Sequence↗
PubMed1992

Behavioral and neurochemical effects of continuous infusion of cocaine in rats.

The ability of continuous intravenous infusion of cocaine (60 mg/kg per day for 11 or 12 days; by osmotic minipump) to alter responses to acute injection of cocaine (20 mg/kg, i.p.; given 24 hr after termination of the infusion by minipump) was tested in conscious, tethered Sprague-Dawley rats. Extracellular levels of cocaine, dopamine and metabolites of dopamine in the striatum were determined by in vivo microdialysis. Locomotor activity and stereotyped behavior were evaluated simultaneously during dialysis sampling. Prior infusion of cocaine blunted the ability of acute challenge with cocaine to increase the efflux of dopamine in the striatum, locomotor activity and stereotypy. Increases in extracellular levels of homovanillic acid in the striatum were significantly greater in cocaine-infused rats than vehicle-infused controls, both prior to and after acute injections of cocaine. However, no differences between these two groups were observed in levels of cocaine in the striatum after acute challenge. Extracellular levels of dopamine in the striatum correlated significantly (P less than 0.05) with stereotypy in both groups but with locomotor activity only in cocaine-infused rats. The results indicate that behavioral tolerance occurred after continuous intravenous infusions of cocaine, that this was correlated with neurochemical tolerance to acute cocaine challenge and that alterations in the metabolism of cocaine did not account for the observed behavioral responses.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Susceptibility to sensitization. II. The influence of gonadal hormones on enduring changes in brain monoamines and behavior produced by the repeated administration of D-amphetamine or restraint stress.

Repeated amphetamine use produces an enduring sensitization of brain dopamine (DA) systems and behavior. Repeated exposure to stress can also produce sensitization, and amphetamine and stress may be interchangeable in this regard. There is, however, enormous individual variation in the susceptibility to sensitization by either stimulants or stress. The purpose of the present study was to determine if endogenous gonadal hormones contribute to individual variation in the sensitization of stereotyped behaviors, locomotion or regional brain monoamine metabolism. It was found that removal of testicular hormones by castration of male rats facilitated the behavioral sensitization produced by either repeated amphetamine treatment or repeated restraint stress, but ovariectomy of female rats was without effect. Prior exposure to amphetamine enhanced striatal homovanillic acid (HVA) levels and dihydroxyphenylacetic acid to DA and HVA to DA ratios in intact female, ovariectomized female and castrated male rats, but not gonadally-intact male rats. As a group, intact males were particularly heterogeneous because they were divisible into two neurochemically distinct subgroups based on their degree of behavioral sensitization, and the other groups were not. It is suggested that individual differences in the sensitization of brain DA systems and behavior produced by repeated exposure to amphetamine or stress may be due in part to individual differences in the concentration of a testicular hormone.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Functional anatomy of occipital lobe seizures: an experimental study in rats.

Small amounts of penicillin were used to create a seizure focus in the primary visual cortex (area 17), extrastriate cortex (area 18 and 18a), and neighboring somatosensory and temporal areas in rats. Autoradiography with 14C-deoxyglucose was used to map the focus and the local cortical and long subcortical circuits. Mild seizures from area 17 were associated with focal spiking without behavioral manifestations. There was restricted utilization of local U-fiber circuits and ipsilateral subcortical visual system nuclei. Stronger seizures filled up the visual cortex and projected into adjacent neocortex and limbic cortex, the contralateral 17-18a border, and additional subcortical nuclei. Seizures originating in the posterior visual cortex were associated with prolonged afterdischarges and stereotyped behavioral manifestations, with spread into the posterior cingulum, the subicular complex, and the bilateral hippocampus. After analyzing the electrographic discharges, behavior, and seizure pathways in each animal, we conclude that ictal symptoms associated with seizures would not be the expression of the function of a cortical focus, but rather of the dysfunction of excessive discharges through many local and long circuits.

Animals↗
PubMed1991

Diltiazem suppresses quinpirole-induced oral stereotypies in haloperidol withdrawn rats.

1. Tardive dyskinesia (TD) is one of the most serious untoward effects of chronic neuroleptic therapy. Dopaminergic receptor sensitization is assumed to be involved in its pathogenesis. 2. Male Wistar rats were administered (b.i.d.) intragastrically haloperidol (2 mg/kg), diltiazem (5 mg/kg), diltiazem plus haloperidol, and water (controls), for 21 days. 3. Forty eight hours after withdrawal the rats were injected ip with 0.3 mg/kg of quinpirole and observed for stereotypic behaviors (rearing, grooming, licking, and tongue protrusions). 4. There was a significant overall between-group difference in the duration of grooming and the number of tongue protrusions. The haloperidol withdrawn rats scored markedly higher than control and diltiazem alone treated rats. 5. Conjoint treatment with diltiazem and haloperidol prevented the increase of tongue protrusion episodes. 6. We conclude that concurrent diltiazem and haloperidol administration can prevent the occurrence of some behavioral manifestations of dopaminergic receptor supersensitivity, including a lingual dyskinesia.

Analysis of Variance↗
PubMed2001

Hypolocomotor effects in rats of capsaicin and two long chain capsaicin homologues.

Capsaicin and its analogue N-arachidonoyl-vanillyl-amine (arvanil) are agonists of vanilloid VR1 receptors, and suppress spontaneous activity in mice through an unknown mechanism. Here, we tested in rats the effect on motor behavior of: (1) capsaicin; (2) N-linoleoyl-vanillyl-amine (livanil) and N-alpha-linolenoyl-vanillyl-amine (linvanil), which, unlike arvanil, have very little affinity for cannabinoid CB1 receptors; and (3) the endocannabinoid anandamide (N-arachidonoyl-ethanolamine), which is a full agonist at both cannabinoid CB1 and vanilloid VR1 receptors. All compounds, administered i.p., dose-dependently (0.1-10 mg/kg) inhibited ambulation and stereotypic behavior and increased inactivity in the open field test. The rank of potency observed in vivo (livanil>capsaicin>linvanil>anandamide) bore little resemblance with the relative potencies in a functional assay for rat vanilloid VR1 receptors (livanil=linvanil>capsaicin>anandamide) and even less with the relative affinities in rat CB1 receptor binding assays (anandamide>livanil>linvanil>capsaicin). The vanilloid VR1 receptor antagonist capsazepine (10 mg/kg, i.p.) blocked the effect of capsaicin but not of livanil or anandamide, whereas the CB1 receptor antagonist (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide.HCl (SR141716A, 3 mg/kg, i.p.) antagonized the actions of the CB1 receptor agonist Delta9-tetrahydrocannabinol, but not of livanil, anandamide or capsaicin. Anandamide occluded the effects of livanil on locomotion, possibly suggestive of a common mechanism of action for the two compounds. Finally, stimulation with capsaicin of cells expressing rat vanilloid VR1 receptors led to anandamide formation. These data suggest that motor behavior can be suppressed by the activation of: (1) vanilloid receptors, possibly via the intermediacy of anandamide; or (2) capsazepine- and SR141716A-insensitive sites of action for anandamide, livanil and linvanil, possibly the same that were previously suggested to mediate arvanil hypokinetic effects in mice.

Animals↗