Stereotyped Behavior In Rats Research Articles

Study of the effect of phosphorylated carboxylic acids new derivatives on the main behavioral disorders in rats in the valproate model of autism

BACKGROUND: Due to the increasing frequency of autism in the population, the complexity of behavioral symptoms, and the need for long-term therapy, it is important to find new safe drugs for the correction of behavioral disorders.
 AIM: Studying the possibility of correcting behavioral changes characteristic of autism in rats in the valproate model of autism using new derivatives of phosphorylated carboxylic acids.
 MATERIAL AND METHODS: The possibility of correcting behavioral disorders in male and female rats in the valproate model of autism was studied with intraperitoneal administration (7 days) of new derivatives from the group of phosphorylated acetohydrazides (B2, C5) and thiosemicarbazide (T8) in doses of 1/100 LD50 on behavioral tests “Elevated Plus Maze”, “Burying Balls”, “Extended Open Field”. Statistical processing was carried out in the GraphPad prism 8.0.1 program using Student's t-test.
 RESULTS: It was found that the most pronounced anxiolytic effect on rats with autism was exerted by the compound 2-[(diphenylphosphoryl)acetyl]-N-phenylhydrazine-1-carbothioamide (T8), increasing by 4.8 times (p=0.033) in females and 4.4 times (p=0.036) in males, the time they spent in open arms in the “Elevated Plus Maze” test. The corrective effect on social behavior in rats with autism was most noted for T8 and B2 [2-ethoxy-2-oxoethanammonium salt (2-ethoxy-2-oxotyl) phenylphosphinic acid], which was characterized by an increase in the time spent with a social object (unfamiliar rat) 6.4 times (p=0.04) and 5.2 times (p=0.039), respectively, in the “Extended open field” method. When assessing the behavior of rats in the valproate model of autism in the “Burying Balls” test, it was found that the use of B2, T8 and C5 reduced the level of stereotypy, reducing the number of buried balls by 1.7 times (p=0.009), 1.5 times (p=0.046 ) and 1.7 times (p=0.011), respectively, compared to rats in the valproate model of autism without treatment.
 CONCLUSION: Derivatives of phosphorylated acetohydrazides and thiosemicarbazide have an anxiolytic effect, correct disturbances in social behavior and reduce the severity of stereotypic behavior in rats in the valproate model of autism.

Application of 18-fluorodeoxyglucose as an indicator of symptom severity in a rat model of tic disorder following treatment with traditional Chinese medicine.

Quantitative evaluation of tic disorders (TDs) is challenging as there are few objective indicators that can be used for the assessment of treatment outcomes. 18F-Fluorodeoxyglucose (FDG) is a radioactive tracer that is able to cross the blood-brain barrier and can be detected by positron emission tomography/CT (PET/CT). In the present study, it was hypothesized that FDG PET/CT scan can be applied to reflect the severity of tic symptoms in a rat TD model, where signals detected in the brain striatum can be used to evaluate the efficacy of tic treatment with traditional Chinese medicine (TCM). A rat model of TD was established by treatment with iminodipropionitrile. Rats were divided into the following four groups (n=10 each): i) Control; ii) TCM; iii) haloperidol; and iv) model only. Observations of stereotypic behavior in rats were subsequently scored and micro-PET/CT was used to evaluate the rate of FDG uptake. Stereotypy scores were found to be significantly higher (P<0.05) in the TD rat model (P<0.05) compared with those in control rats. Both stereotypy scores (P<0.05) and standardized FDG uptake values (SUV; P<0.05) were revealed to be significantly reduced in the TD model rats after treatment with TCM or haloperidol. SUV correlated positively with stereotypy score (R=0.926; P<0.05) and the SUV scores were found to be significantly different among control group, TCM group, haloperidol group and model only group (P<0.05). These data suggest that the application of FDG in the striatum can be used to evaluate the effectiveness of TCM treatment for TDs.

Neuropeptide S attenuates methamphetamine-induced stereotyped behavior in rats

Effective therapies for Methamphetamine (METH) induced stereotyped behavior are still being explored. It is unclear whether Neuropeptide S (NPS) is involved in the mechanism of METH-induced stereotyped behavior. In the contemporary behavioral study, pretreatment with NPS reduces stereotyped circling significantly, but didn’t have any impact on the total incidence of stereotypy and stereotyped sniffing and biting induced by METH (10 mg/kg). When METH (10 mg/kg) was administered to rats, the level of NPS in the cerebrospinal fluid was not affected, but pretreatment with NPS reversed METH-induced glutamate release in the hippocampus and striatum. The findings suggest that NPS receptor system is likely to involve in the METH-overdose-induced behaviors.

Anti-Psychotic Activity of Aqueous Root Extract of Hemidesmus indicus: A Time Bound Study in Rats.

Psychosis is a neurological disorder, which is usually defined as the &amp;quot;loss of contact with reality.&amp;quot; As medicine 'Hemidesmusindicus' holds a reputed place in all systems of medicine in India. It is given in the form of infusion, fine particles, or syrup. It is also a component of several medicinal preparations. The present research work is pertaining to find out an anti-psychotic activity of an aqueous root extract of Hemidesmusindicus- a time bound study in rats. In the present study, the dried roots of Hemidesmusindicus were crushed to a coarse powder and extracted with water under reflux for 36 hours to obtain the aqueous extract of roots of Hemidesmusindicus (AERHI). The extract was reconstituted in 2% aqueous tragacanth just before use and administered orally at a dose 0f 100 mg/kg, 300 mg/kg and 500 mg/kg. In a single dose study, the parameters were assessed after oral administration of the single dose of the AERHI, whereas in a multiple dose study, the animals daily received the suitable oral dose of the AERHI for a period of 30 days. The parameters were assessed on the 15th and 30th day. The antipsychotic activity was screened using Apomorphine induced Stereotyped behavior in rats and Haloperidol induced catalepsy models were used. In Apomorphine induced Stereotyped behavior inhibition of the Stereotyped behavior was considered to be anti-psychotic activity and in Haloperidol induced catalepsy, we observed whether the AERHI potentate or attenuate the catalepsy in rats. In this study, the extract of Hemidesmusindicus significantly inhibited the stereotyped behavior induced by apomorphine in rats and also potentiate the catalepsy induced by haloperidol, thereby showing its anti-psychotic activity. All these observations imply that Hemidesmusindicus extract possesses anti-psychotic activity in experimental animals.

Antipsychotic activity of embelin isolated from Embelia ribes: A preliminary study

BackgroundEmbelia ribes is claimed in Indian traditional medical practice to be useful in the treatment of nervous diseases. Embelin, an alkyl substituted hydroxy benzoquinone, is a major active constituent of E. ribes. The present preliminary study was intended to evaluate antipsychotic activity of embelin against apomorphine-induced climbing behaviour in mice and stereotyped behaviour in rats. MethodsTwo doses of embelin (5 and 10mg/kg) were administered once daily for 15days before exposure to apomorphine. On the concluding day of pre-treatment, after apomorphine-injection, the rodents were assessed for climbing and stereotyped behaviours according to the published scoring system. Thereafter, neurotransmitters (dopamine, noradrenaline and serotonin) levels were estimated in rodent brains. ResultsEmbelin pre-treatment significantly inhibited apomorphine-induced climbing and stereotyped behaviours in mice and rats, respectively. Further, embelin also statistically reversed elevated levels of dopamine, noradrenaline and serotonin neurotransmitters in the brain of mice and rats. Embelin showed more significant results at high dose (10mg/kg) than low dose (5mg/kg) in both the tested models. ConclusionConsidering the present pharmacological profile of embelin, it is suggested that embelin possesses antipsychotic activity in the treatment of psychotic disorders. However, further research is warranted for evaluating its exact mechanism of action.

Fatty liver-induced changes in stereotypic behavior in rats and effects of glucagon-like peptide-1 analog on stereotypy

Although understanding the relation between psychotic behavior and immune abnormalities has been the focus of research for many years, it remains to be elucidated whether the changes in cytokine levels are part of etiology or a result of the stress associated with the disorder. In accordance with previous studies on changes in cytokine levels due to metabolic changes and psychosis, we hypothesized that fatty liver may potentiate apomorphine-induced stereotypy in a rodent model and that a synthetic glucagon-like peptide-1 analog exenatide would ameliorate this effect. In this study, 18 male Sprague Dawley albino mature rats were used. We induced hepatosteatosis in these rats by feeding them with 30% fructose dissolved in drinking water for 8 weeks. The animals were divided into three groups, namely, the normal group, the intracerebroventricular (ICV) exenatide group, and the ICV NaCl group. Apomorphine-induced stereotypic behavior test was performed in all groups and the liver was removed for histopathological examination after all the rats were euthanized. In the nonalcoholic fatty liver (NAFL) group, stereotypy scores were significantly increased compared with the control group rats (p < 0.00001). A significant decrease in stereotypy scores were observed in the ICV exenatide group with NAFL when compared with the ICV saline group with NAFL (p < 0.005). In addition, brain malondialdehyde and tumor necrosis factor-α levels decreased in the ICV exenatide group. The results of this study showed that fatty liver enhances the effect of apomorphine on stereotypy, which was reversed by exenatide possibly by antioxidant and anti-inflammatory effects.

Effect of Sodium Valproate Pretreatment on Apomorphine and Dexamphetamine Induced Stereotyped Behavior in Rats

Sodium valproate, a broad spectrum antiepileptic, elevates the brain GABA levels. Studies have suggested regulatory role of GABA on dopaminergic neurons, which is evident by behavioral studies in animals that reveal functional interaction between GABAergic and DAergic systems. Hyperfunctioning of DAergic system in rats is responsible for occurrence of stereotyped behavior (SB) in them. Drugs like apomorphine (Apo) and amphetamine induce SB by acting directly or indirectly. GABA, by acting at different sites has shown to influence the dopaminergically mediated behaviors. Hence the study was taken up to investigate the effect of sodium valproate pretreatment on apomorphine and dexamphetamine induced SB in rats. Pretreatment with 100 to 400mg/kg sodium valproate did not antagonize the apomorphine induced SB, however pretreatment with 100 to 400mg/kg sodium valproate significantly antagonized SB induced by 10 & 15mg/kg dexamphetamine.

Pharmacological Profile of Lurasidone, a Novel Antipsychotic Agent with Potent 5-Hydroxytryptamine 7 (5-HT7) and 5-HT1A Receptor Activity

Lurasidone [(3aR,4S,7R,7aS)-2-[(1R,2R)-2-[4-(1,2-benzisothiazol-3-yl)piperazin-1-ylmethyl]cyclohexylmethyl]hexahydro-4,7-methano-2H-isoindole-1,3-dione hydrochloride; SM-13496] is an azapirone derivative and a novel antipsychotic candidate. The objective of the current studies was to investigate the in vitro and in vivo pharmacological properties of lurasidone. Receptor binding affinities of lurasidone and several antipsychotic drugs were tested under comparable assay conditions using cloned human receptors or membrane fractions prepared from animal tissue. Lurasidone was found to have potent binding affinity for dopamine D(2), 5-hydroxytryptamine 2A (5-HT(2A)), 5-HT(7), 5-HT(1A), and noradrenaline alpha(2C) receptors. Affinity for noradrenaline alpha(1), alpha(2A), and 5-HT(2C) receptors was weak, whereas affinity for histamine H(1) and muscarinic acetylcholine receptors was negligible. In vitro functional assays demonstrated that lurasidone acts as an antagonist at D(2) and 5-HT(7) receptors and as a partial agonist at the 5-HT(1A) receptor subtype. Lurasidone showed potent effects predictive of antipsychotic activity, such as inhibition of methamphetamine-induced hyperactivity and apomorphine-induced stereotyped behavior in rats, similar to other antipsychotics. Furthermore, lurasidone had only weak extrapyramidal effects in rodent models. In animal models of anxiety disorders and depression, treatment with lurasidone was associated with significant improvement. Lurasidone showed a preferential effect on the frontal cortex (versus striatum) in increasing dopamine turnover. Anti-alpha(1)-noradrenergic, anticholinergic, and central nervous system (CNS) depressant actions of lurasidone were also very weak. These results demonstrate that lurasidone possesses antipsychotic activity and antidepressant- or anxiolytic-like effects with potentially reduced liability for extrapyramidal and CNS depressant side effects.

Role of nigral NFκB p50 and p65 subunit expression in haloperidol-induced neurotoxicity and stereotyped behavior in rats

Long-term use of typical neuroleptics such as haloperidol may be limited by unwanted motor side effects like tardive dyskinesia (TD) characterized by repetitive involuntary movements, involving the mouth, face and tongue. TD generally persists after haloperidol withdrawal indicating long lasting changes in brain function that are no longer related to the presence of the drug. The precise mechanisms of the neuronal toxicity induced by haloperidol are poorly understood. Haloperidol has been shown to induce the expression of the transcription factor nuclear factor-κB (NFκB). NFκB resembles a heterodimer protein composed of a 50 and a 65 kDa subunits and the role of the NFκB subunits on haloperidol-induced toxicity remains still unknown. The aim of the present study is to investigate the role of the p65 and p50 subunits of NFκB on the toxicity induced by chronic haloperidol administration in an experimental model of TD. Rats were treated for 21 days with: haloperidol (1 mg/kg), clozapine (1 mg/kg) or saline. Apomorphine-induced stereotyped behavior was evaluated. Striatal expression of the dopamine transporter (DAT) and the nigral expression of the NFκB p65 and p50 subunits were measured by Western Blot. Haloperidol, but not clozapine, increased stereotyped behavior associated to a decreased striatal DAT expression ( p < 0.01). Haloperidol did not modify the nigral expression of the p65 subunit whereas clozapine decreased it ( p < 0.01). Both drugs induced a significant decrease in the nigral expression of the NFκB p50 ( p < 0.05 and p < 0.01, respectively). The decrease in nigral expression of the p50 subunit may increase the vulnerability of the dopaminergic neurons to a possible neurotoxic effect of p65 subunits in the haloperidol-treated rats.

Effects of amphetamine and sydnocarb on dopamine release and free radical generation in rat striatum

Microdialysis technique was used to compare the effects of four repeated intraperitoneal administrations of two psychostimulant drugs, d-amphetamine and sydnocarb, at the equimolar doses 5 and 23.8 mg/kg, respectively, on the extracellular level of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and hydroxyl radicals (·OH) in the dorsal striatum of freely moving 3-month-old male Wistar rats 250–300 g in weight. d-Amphetamine caused immediate increase of DA concentration up to 950% with quick decline towards baseline values thereafter, followed by much less increase after further injections. Sydnocarb elicited moderate elevation in DA level achieving 400% after the fourth injection. d-Amphetamine induced deep decrease in DOPAC concentration, while sydnocarb caused its increase after the first and second dosing. Both drugs enhanced generation of ·OH, the effect of d-amphetamine was more pronounced. d-Amphetamine induced more intensive stereotyped behavior in rats compare to sydnocarb. It is concluded that the psychostimulant action of sydnocarb is accompanied by facilitation of the central dopaminergic transmission in rat neostriatum and followed by less pronounced neurotoxic effect than that of d-amphetamine.

Dextrorotatory opioids induce stereotyped behavior in Sprague-Dawley and Dark Agouti rats.

Dextromethorphan and dextrorphan elicited a stereotyped behavioral syndrome in rats indistinguishable from that produced by PCP and other non-competitive NMDA antagonists. The rank order of potency for the induction of stereotyped behavior in male Sprague-Dawley rats was: MK-801>PCP>(+/-)cyclazocine>dextrorphan>(+/-)ketamine>dextromethorphan. These behavioral potencies were significantly correlated (0.91; P<0.05) with their respective affinities for high affinity [3H]dextrorphan-labelled NMDA receptors in rat forebrain membranes. To address the propensity of dextromethorphan to induce stereotyped behavior, dextrorotatory-opioid induced stereotypies were investigated in female Dark Agouti and female Sprague-Dawley rats. The female Dark Agouti lacks CYP2D1, the cytochrome P450 enzyme which catalyses the oxidative O-demethylation of dextromethorphan to dextrorphan. No differences were observed in either potency or time to peak effect for dextromethorphan to induce stereotyped behavior in the rat strains, suggesting that the affinity of dextromethorphan for NMDA receptors adequately accounts for its ability to induce stereotyped behavior. Female Dark Agouti rats were, however, more sensitive to the effects of dextrorphan, which may reflect differences in the ability of this strain to metabolize dextrorphan. We find no evidence to suggest that dextromethorphan produces a behavioral syndrome in rats that is distinct from that induced by dextrorphan. The commonality between the pharmacologic profiles of these compounds suggests that the abuse potential of dextromethorphan containing antitussive preparations is related to the non-competitive NMDA antagonist activity of dextromethorphan and its metabolites.

Sigma 1 Receptor Subtype Does Not Interact With Stereotyped Behaviors in Rats

In the present study, we clearly showed that the sigma 1 receptor subtype did not interact with the induction of stereotyped behaviors in rats. Namely, (+)- N-allylnormetazocine [(+)-SKF-10,047] (5.0, 10.0, and 20.0 mg/kg, SC), a traditional sigma receptor ligand that has affinities for the sigma 1 receptor subtype and the N-methyl-D-aspartate (NMDA)/phencyclidine (PCP) receptor channel complex, markedly produced PCP-like stereotyped behaviors, such as head weaving, turning, and backpedaling, in rats. On the contrary, 1-(3,4-dimethoxyphenyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA4503), a potent and selective sigma 1 receptor agonist, did not produce these behaviors. Additionally, PCP-induced stereotyped behaviors were significantly augmented by (+)-SKF-10,047, but not by SA4503. We thus suggest that the induction of PCP-like stereotyped behaviors elicited by (+)-SKF-10,047 closely interacts with NMDA/PCP receptor channel complex but not with the sigma 1 receptor subtype.

The atypical antipsychotic profile of NRA0045, a novel dopamine D4 and 5-hydroxytryptamine2A receptor antagonist, in rats.

1. The atypical antipsychotic profile of (R)-(+)-2-amino-4-(4-fluorophenyl)-5-[1-[4-(4-fluorophenyl)-4-oxobutyl] pyrrolidin-3-yl] thiazole (NRA0045), a potent dopamine D4 and 5-hydroxytryptamine (5-HT)2A receptor antagonist, was examined in rats. 2. Spontaneous locomotor activity was decreased dose-dependently with i.p. administration of clozapine (ED50 3.7 mg kg-1), haloperidol (ED50 0.1 mg kg-1) and chlorpromazine (ED50 0.9 mg kg-1), whereas inhibition of this type of behaviour induced by i.p. administration of NRA0045, at doses up to 10 mg kg-1, did not exceed 50%. 3. Locomotor hyperactivity induced by methamphetamine (MAP, 2 mg kg-1, i.p.) in rats (a model of antipsychotic activity) was dose-dependently antagonized by NRA0045 (ED50 0.4 mg kg-1, i.p., and 0.3 mg kg-1, p.o., respectively), clozapine (ED50 0.3 mg kg-1, i.p. and 0.8 mg kg-1, p.o., respectively), haloperidol (ED50 0.02 mg kg-1, i.p. and 0.1 mg kg-1, p.o., respectively), chlorpromazine (ED50 0.3 mg kg-1, i.p. and 3.3 mg kg-1, p.o., respectively). In contrast, the MAP (3 mg kg-1, i.v.)-induced stereotyped behaviour in rats (a model of extrapyramidal symptoms) was not affected by NRA0045 or clozapine, at the highest dose given (30 mg kg-1, i.p.). Haloperidol (ED50 0.3 mg kg-1, i.p.) and chlorpromazine (ED50 4.8 mg kg-1, i.p.) strongly blocked the MAP-induced stereotyped behaviour. NRA0045 and clozapine selectively blocked behaviour associated with activation of the mesolimbic/mesocortical dopamine neurones rather than nigrostriatal dopamine neurones. 4. Extracellular single-unit recording studies demonstrated that MAP (1 mg kg-1, i.v.) decreased the firing rate in the substantia nigra (A9) and ventral tegmental area (A10) dopamine neurones in anaesthetized rats. NRA0045 completely reversed the inhibitory effects of MAP on A10 dopamine neurones (ED50 0.1 mg kg-1, i.v.), whereas the inhibitory effects of MAP on A9 dopamine neurones were not affected by NRA0045, in doses up to 1 mg kg-1 (i.v.). Clozapine completely reversed the inhibitory effects of MAP on A10 dopamine neurones (ED50 1.9 mg kg-1, i.v.) and on A9 dopamine neurones (ED50 2.5 mg kg-1, i.v.). Haloperidol completely reversed the inhibitory effects of MAP on A10 (ED50 0.03 mg kg-1, i.v.) and on A9 dopamine neurones (0.02 mg kg-1, i.v.). NRA0045, like clozapine, was more potent in reversing the effects of MAP on A10 than A9 dopamine neurones. 5. Prepulse inhibition (PPI) is impaired markedly in humans with schizophrenia. The disruption of PPI in rats by apomorphine (0.5 mg kg-1, s.c.) was reversed significantly by NRA0045 (3 mg kg-1, i.p.), clozapine (3 mg kg-1, i.p.) and haloperidol (0.3 mg kg-1, i.p.). 6. Phencyclidine (PCP) elicits predominantly psychotic symptoms in normal humans and in schizophrenics. NRA0045 (0.03-0.3 mg kg-1, i.p.) and clozapine (0.1-1 mg kg-1, i.p.) significantly and dose-dependently shortened the PCP(1.25 mg kg-1, i.p.)-induced prolonged swimming latency in rats in a water maze task, whereas haloperidol (0.01-0.1 mg kg-1, i.p.) did not significantly alter swimming latency. 7. These findings suggest that NRA0045 may have unique antipsychotic activities without the liability of motor side effects typical of classical antipsychotics.

P-211 - Effect of diabetes on methamphetamine-induced stereotyped behavior in rats

P-211 - Effect of diabetes on methamphetamine-induced stereotyped behavior in rats

Suppression of psychoactive effects of cocaine by active immunization.

Cocaine is a powerfully addictive substance and new strategies are needed to treat its abuse. Generating an active immunization to cocaine offers a means of blocking the actions of the drug by preventing it from entering the central nervous system, and should have fewer side effects than treatments based on manipulation of central neurotransmitter function. The design and preparation of a cocaine immunogen requires special regard for the stability of cocaine both free and as a haptenic determinant. Immunochemistry and a well defined behavioural model were brought together to address the problem of inactivation of the psychostimulant actions of cocaine. We report here that active immunization with a new, stable cocaine conjugate suppressed locomotor activity and stereotyped behaviour in rats induced by cocaine but not by amphetamine. Moreover, following acute injection of cocaine, levels of cocaine in the striatum and cerebellum of the immunized animals were lower than those of control animals. These results suggest that immunopharmacotherapy may be a promising means by which to explore new treatments for cocaine abuse.

Application of the common marmoset to pharmacological studies

Application of the common marmoset to pharmacological studies was reviewed, especially employment of the animal as a model of Parkinson's disease were presented. The common marmoset is one of the New World monkeys with a body weight of 300-350 g. It is small enough to be easily handled and to be kept as a group in a room. In the fields of pharmacology, it has been used in studies of plasma renin activity inhibitors, lipoprotein, memory/learning, obstetrics, transplantation, toxicology, anxiolytic agents and virology/immunology. We showed that the common marmoset was a useful animal for studies on Parkinson's disease, dopamine metabolism by microdialysis and nausea/vomiting. The common marmoset was sensitive to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and developed permanent parkinsonism after MPTP injection. MPTP-treated common marmosets showed tremor and akinesia, and it remarkably responded to antiparkinsonian agents. A dopamine D1 agonist, which caused stereotyped behavior in rats, did not reverse parkinsonism in humans. We showed this agent did not have any antiparkinsonian effects on MPTP-treated common marmosets. MAO has subtypes, A and B, that have differences of distribution in different species. MAO type B inhibitors were applied for the treatment of Parkinson's disease. MAO subtype B inhibitors do not cause any change in behavior or extracellular concentration of dopamine or its metabolites in rodents. In MPTP-treated common marmosets, however, administration of a MAO type B inhibitor increased the antiparkinsonian effects of levodopa and decreased dopamine metabolites. The common marmoset is a suitable animal for the study of MAO type B inhibitors.

Early postnatal antidepressant treatment and juvenile stereotyped behaviour in rats

The effect of antidepressants on stereotyped behaviour in rats during development was examined. Rats were injected s.c. once a day from the 6th to the 22th day after birth with 0.9% sodium chloride, with desipramine 5 mg/kg body weight, with nomifensine 10 mg/kg, or with zimelidine 25 mg/kg. Stereotyped behaviour was assessed when the rats were 1 month and 2 months of age. Desipramine intensified and prolonged apomorphine 0.5 mg/kg induced stereotyped behaviour at 1 month but not at 2 months of age. Nomifensine and zimelidine did not affect stereotyped behaviour at either 1 month or 2 months of age. Thus, 2-week treatment with desipramine during early development was shown to increase stereotyped behaviour at a juvenile age.

Efeitos comportamentais e bioquímicos da xilazina: possíveis interações entre os sistemas noradrenérgico e dopaminérgico centrais

Alguns efeitos comportamentais e bioquímicos da xilazina foram estudados em ratos e camundongos. Os resultados mostraram que a xilazina: a) diminuiu a atividade geral de ratos e camundongos observados em campo-aberto; b) foi incapaz de produzir catatonia e suprimiu este comportamento induzido pelo haloperidol em camundongos; c) potencializou o comportamento estereotipado induzido pela apomorfina em ratos; d) aumentou os níveis cerebrais de noradrenalina, porem não alterou aqueles de dopamina. Estes resultados foram discutidos considerando-se ação da xilazina em sislemas noradrenérgicos centrais e da interação entre sistemas noradrenérgicos e dopaminérgicos centrais.

Effect of fluctuating currents on the time course of apomorphine-induced stereotypy in rats

The external rhythmogenic influence (repeated fluctuation low intensity) disorganized the time-course and attenuated the apomorphine-induced stereotyped behavior in rats. A decrease in the number of 4-9-minute waves on chronograms in comparison with control an animals indicated reduction of stability of the pharmacological response and the rapid formation of tolerance to the drug.

O-107 - Effect of risperidone on phencyclidine (PCP)-induced stereotyped behavior in rats: Comparison with haloperidol and ritanserin.

O-107 - Effect of risperidone on phencyclidine (PCP)-induced stereotyped behavior in rats: Comparison with haloperidol and ritanserin.