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The effects of essential oil of Croton zehntneri (Euphorbiaceae), orally administered were studied on behavioral parameters using rats and mice. The oil suspension did not modify pentobarbital induced-hypnosis, stereotypic behavior, catalepsy and amphetamine-induced hypermotility. The open-field behaviors were decreased and the minimal convulsant dose of pentylenetetrazole was increased.
Subchronic treatment with the dopamine agonist apomorphine produces a sensitization to the stereotypic effects of subsequent apomorphine challenge. The present study investigated the effects of this subchronic treatment on apomorphine induced stereotypic behavior and striatal dopamine synthesis, release, metabolism, and D2 receptor binding. The pretreatment, which enhanced the behavioral response to apomorphine challenge, also elevated basal dopamine synthesis and metabolism, but left the ability of a challenge dose of apomorphine to inhibit dopamine synthesis and metabolism unaltered. Thus, ongoing dopamine synthesis and extracellular levels of metabolites would be higher following apomorphine challenge in animals treated subchronically with the agonist. In contrast, neither synaptosomal dopamine release in response to depolarizing stimuli nor the density of D2 dopamine receptors was altered by the treatment. Overall, the results suggest that, while we did not find evidence of autoreceptor desensitization per se, apomorphine treatment may result in enhanced extracellular dopamine levels following dopamine agonist challenge to provide a greater stimulation of an intact dopamine receptor system.
The administration of nafadotride, given at doses known to block the D3 dopamine receptors (0.75, 1.5, 3 mg/kg i.p.) increased locomotor activity both in naive and habituated rats and counteracted the hypothermia but not the hypomotility induced by a low dose of the putative D3 dopamine agonist (+/-)-7-hydroxy-2-(di-N-propylamino)-tetralin (7-OH-DPAT; 0.04 mg/kg). Nafadotride did not antagonize either the motor effects induced by different doses of the D2 agonist quinpirole (0.05 and 0.3 mg/kg) or the hypermotility induced by 7-OH-DPAT given at a dose (0.32 mg/kg) stimulating D2 dopamine receptors. The same nafadotride doses potentiated the grooming behavior induced by the D1 dopamine agonist SKF 38393 (10 mg/kg i.p.) as well as the stereotyped response to the D1/D2 agonist apomorphine (0.5 mg/kg s.c.). Stereotyped behavior was also observed in rats concomitantly treated with nafadotride and the D2 agonist quinpirole. As the activation of D1 dopamine receptors plays an important role in the occurrence of stereotypies, the results suggest that the blockade of D3 receptors by nafadotride could have favored D1/D2 dopamine receptor-mediated behaviors by potentiating D1 receptor function.
Differentiating seizures from pseudoseizures frequently is challenging in very young children manifesting repetitive, stereotypic behavior. Using video electroencephalographic recording, we evaluated 60 patients, younger than 10 years of age, with episodic signs and symptoms believed to be seizures despite repeatedly normal routine electroencephalograms. Nine patients (15%) had simple partial and atypical absence seizures. Twenty-four patients (40%) had pseudoseizures presenting as rhythmic movements or staring. Pseudoseizure frequency was greater than the frequency of true seizures; brief staring episodes were common. Motor pseudoseizures usually were of longer duration than true seizures and could be brought on with verbal encouragement. Furthermore, the stereotypic motor presentations were quite different from those of true motor seizures but were difficult to recognize from historic, clinical, and routine electroencephalographic data. Symptomatic patients can be clinically diagnosed by analyzing confirmed episodes with video electroencephalography.
Rates of local cerebral glucose utilization were measured by means of the quantitative autoradiographic 2-[14C]deoxyglucose technique in conscious rats following the acute administration of D-amphetamine (0.2-5.0 mg/kg, i.v.). Changes in locomotor and stereotypic behavior in similarly treated rats were examined as well. Administration of low doses (0.2 and 0.5 mg/kg) of amphetamine resulted in increased locomotor activity, accompanied by elevations in glucose utilization limited mainly to the nucleus accumbens. A moderate dose of D-amphetamine (1.0 mg/kg) produced locomotion and stereotypic sniffing. Metabolic activity at this dose was increased in the nucleus accumbens, throughout neocortical areas, and in components of the extrapyramidal system. A high dose of amphetamine (5.0 mg/kg) produced stereotypic gnawing and licking and was associated with significant increases in glucose utilization in the extrapyramidal system, most prominently in the subthalamic nucleus. These data demonstrate that the acute administration of D-amphetamine produces effects on local cerebral glucose utilization and on behavior that differ with dose. The results also show a strong coupling between locomotion and the level of metabolic activity in the nucleus accumbens and demonstrate that the different forms of stereotypic behavior elicited by high and moderate doses of amphetamine are correlated with distinct patterns of distribution of local cerebral glucose utilization, indicating mediation by different neuronal circuits.
Ten rats, serving as their own controls, were tested for hyperactivity (HyA) (by number of turns of an activity wheel cage) and stereotyped behavior (SB). The animals were given one week each of acclimation to the cages, saline, cocaine (19 mg/kg in 1 cc/kg saline), rest, two weeks on LiCl, and a week on LiCl plus the same dose of cocaine. LiCl produced a nonsignificant decrease of HyA and significantly decreased cocaine SB. The same procedure was duplicated using two different doses of cocaine in five animals each with identical results. The author concludes that Li seems to inhibit cocaine effects in animals and suggests a potential area of research for the use of Li in humans.
Rats given a subcutaneous injection of beta-phenylethyl-amine (PEA) (30 or 60 mg/kg) showed stereotyped behavior and autonomic effects which were suppressed by LiCl. Inhibition of Type A MAO by clorgyline or Lilly 51641 (2 or 8 mg/kg) or of Type B MAO by l-deprenyl (2 or 8 mg/kg) counteracted the suppressant effects of LiCl on PEA-behavior. The findings suggest that both Type A MAO and Type B MAO play a role in the effects of LiCl on PEA-behavior.
Transcerebral microdialysis was used to evaluate the effect of a psychostimulant drug, sydnocarb (3-(beta-phenylisopropyl)-N-phenylcarbamoylsydnonimine), on the extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the dorsal striatum and nucleus accumbens of freely moving rats. Sydnocarb dose dependently (4.4, 8.75 and 17.5 mg/kg, i.p.) induced a relatively modest (up to 350% of control) and long-lasting (up to 6 h) increase in dopamine extracellular level in the rat dorsal striatum. The drug at 8.75 mg/kg, i.p., produced an approximately similar increase in dopamine efflux in the dorsal striatum and in the nucleus accumbens of freely moving rats. Sydnocarb had no effect on DOPAC or HVA extracellular levels in the rat basal ganglia in vivo at any dose studied. It is important that the drug increased the efflux of dopamine in a tetrodotoxin-sensitive and Ca2+-dependent manner. Measurements of behavioral parameters in non-operated rats revealed that sydnocarb markedly increased locomotor activity and induced stereotyped behavior. These data suggest that the stimulant action of sydnocarb is accompanied by a facilitation of central dopaminergic transmission involving an increase in Ca2+-dependent vesicular dopamine efflux.
The effects of calcium channel entry blockers on cocaine and amphetamine-induced behavioral responses were investigated. Cocaine and amphetamine produced dose-dependent increases in locomotor activity and stereotyped behavior with a maximum response at 40 and 1.2 mg/kg, respectively. The 1,4-dihydropyridine nimodipine and the benzothiazepine diltiazem were more effective in inhibiting cocaine (20 mg/kg)-induced responses than amphetamine (0.6 mg/kg)-induced responses. At doses of cocaine and amphetamine that caused seizures and death, nimodipine, nitrendipine and diltiazem did not offer any protection; rather, they potentiated the toxicities produced by these psychomotor stimulants.
In this study concomitant changes of behavioral and biochemical responses in rats repeatedly treated with SCH 23390 were evaluated. Apomorphine-induced stereotyped behavior was increased in D1-supersensitive rats, in contrast no change in the behavioral response to the pure D1-agonist SKF 38393 was detected. Parallel biochemical studies indicated that the enhancement in striatal dopamine (DA) metabolite concentration due to the administration of spiroperidol plus SKF 38393 was not potentiated in SCH 23390 repeatedly treated rats. The results show that the expression of D1-supersensitivity could depend on the stimulation of D2-receptors.
Viruses have been proposed to play a role in the pathogenesis of schizophrenia; however, the mechanisms by which infection could cause the affective, cognitive, and movement disorders of schizophrenia are not understood. The neurotropic RNA virus, Borna disease (BD) virus, linked to schizophrenia by serologic studies, causes movement and behavior disorders in a wide variety of mammalian and bird hosts. BD rats have hyperactivity and stereotyped behaviors similar to those that follow neurotoxic or electrolytic lesions in frontal cortex or its catecholamine afferents in rats. BD rats have high levels of viral nucleic acid in the prefrontal cortex (PFC), abnormal mesocortical dopamine activity (elevated levels of DOPAC in PFC), yet no alteration in specific binding of D1 or D2 receptor radioligands in PFC. Since frontal lobe dysfunction is frequently reported in schizophrenia, the BD rat model may provide insights into pathogenesis and management of this debilitating psychiatric disease.
Time-based lag sequential analyses were conducted on 23 topographies of challenging behavior shown by five young people with severe mental retardation across two settings. Potential behavioural functions were identified for 21 of the 23 behaviors. Responses classes, including two or more distinct behaviors, were identified for four of the five participants. Two participants showed evidence of two functionally distinct response classes; for one person each response class included both self-injurious and stereotypic behaviors. For 9 of the 11 behaviors for which data were available, the hypothesised function of behaviors was consistent across settings. For one person, data suggested that the function of one self-injurious behavior was contextually determined. Cross-validation with brief experimental analyses resulted in agreement on the general behavioral function for 12 of the 14 instances in which both approaches positively identified a potential function for a behavior. Implications for future research and practice are discussed.
Ketamine in a dose of 100 mg/kg (IP) produced stereotypic behavior and vigorous rotation in adult male Sprague-Dawley rats. The first rotation phase, accompanied by head swinging, was short and terminated by the anesthetic phase which lasted 20-30 min. The second rotation phase began 1-3 min after the end of the anesthetic phase. A single dose of GABA-T inhibitors, gamma-vinyl GABA (1200 mg/kg, IP) or gamma-acetylenic GABA (100 mg/kg, IP) administered 4 hours prior to ketamine, shortened the first rotation phase, increased the anesthetic phase, changed the pattern of postanesthetic rotation and reduced total and net rotation scores. Picrotoxin (3 mg/kg) given 10 min prior to ketamine tended to act in the opposite direction although none of its effects reached statistical significance.
Saline-treated and amphetamine-treated (7 mg/kg, ip, immediate) male rats from a Sprague-Dawley substrain were observed in two test environments designed to elicit different investigative responses in normal rats. Snout contact with the substrate was generated by placing the rat in a small enclosed cage. Absence of snout contact was induced by placement of the rat on a square elevated platform. Detailed ethological records were kept of locomotion, rearing, sitting, grooming, gnawing, and sleeping throughout the 90-min session. Amphetamine-treated rats incorporated environmentally contingent bodily postures into their forms of stereotyped behavior. The postures were characteristic of those evinced initially by the saline-treated rats in the same test environment. The control rats showed appropriate changes in their investigative behavior when the apparatus was changed at 10 and at 30 min postinjection. The amphetamine-treated rats, however, were completely unresponsive to such changes at 30 min and only partially so at 10 min postinjection. It was concluded that there is a temporal gradient of decreasing readiness to modify repetitive behavior after a single, large dose of amphetamine.
The author contended opposite pharmacological effects resulting from lithium and amphetamine. Three groups, each one consisting of four rats, were put on chronic lithium condition to measure its effects on amphetamine hyperactivity. This condition was effected after appropriate handling and saline control periods and the baselines for drug activity were measured. In young rats (150-200g), lithium significantly decreased d-amphetamine hyperactivity (and probably other effects, like anorexia) while producing little effect on amphetamine stereotyped behavior (ASB). If confirmed, this fact may prove of marked importance in further localizing and studying the pharmacology of lithium. However, this observation was true in only three rats of the first group. All other rats, of the older group or of the other strain, showed only ASB, a fact that also deserves further study because it seems to contradict previous important reports.
Male albino Wistar rats were injected intraperitoneally with saline solution (1.0 ml/kg) or a-methyl-paratyrosine (50 mg/kg) once or daily X 7 and methamphetamine (10 mg/kg) was injected 3 hr or 24 hr after the last injection of these drugs. Stereotyped licking and biting activity were scored during 120 min after methamphetamine injection and, in parallel brain dopamine levels were measured. Methamphetamine given 3 hr after single or repeated administrations of alpha-methyl-para-tyrosine was not effective for stereotyped behavior and brain dopamine levels in similarly treated rats decreased markedly in comparison with saline-treated rats. Methamphetamine 24 hr after repeated administration of alpha-methyl-para-tyrosine clearly induced stereotypies and brain dopamine levels in these rats did not differ from saline-treated rats. The results suggest a possible role of brain dopamine on "methamphetamine-stereotypies".
An intensification of a swimming behavior with an increase in the proportion of active swimming and limitation of the duration of immobilization was found in rats following bilateral electrolytic destruction of the suprachiasmatic nuclei of the hypothalamus. The restructuring of the temporal dynamics of swimming is manifested in a limitation of the rhythmological index of depressivity. The animals with ablated nuclei demonstrate more pronounced behavioral disturbances in response to the introduction of fenamin and a slowing of the minute fluctuations in the dynamics of stereotypic behavior.
The purpose of this study was to examine the binding and behavioral effects mediated by PCP and sigma receptors in the rat. From the radioreceptor assays, it was possible to characterize two binding sites that interact with PCP and sigma ligands. The two sites, a PCP and sigma receptor, could be differentiated based on drug selectivity and potency. In the behavioral assays, MK-801, which bound preferentially to the PCP receptor, and 1,3-di-0-tolylguanidine, which bound preferentially to the sigma receptor, induced sniffing, rearing, circling, backpedaling, and weaving behavior. These results indicate that there are distinct PCP and sigma receptors that are both involved in mediating stereotyped behavior and ataxia in the rat.