Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Stereotyped Behavior”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 973 records · Page 54Linked to original sources
PubMed2003

Central inhibitory activity of the aqueous extract of Crinum giganteum.

The aqueous extract of Crinum giganteum given intraperitoneally at doses of 6.25, 12.5 and 25 mg/kg in rats prolonged the duration of pentobarbital sleeping time and in mice reduced spontaneous motor activity, decreased the exploratory activity and attenuated amphetamine-induced stereotype behavior. The intraperitoneal and oral preliminary LD(50) in mice were found to be 627 and 1468 mg/kg, respectively. The data obtained suggest that the aqueous extract of C. giganteum contains some biologically active principles with sedative activity.

Administration, Oral↗
PubMed1987

D1 dopamine receptor activation required for postsynaptic expression of D2 agonist effects.

D1 and D2 dopamine receptors exert synergistic effects on the firing rates of basal ganglia neurons and on the expression of stereotyped behavior in rats. Moreover, the ability of D2 agonists to induce changes in basal ganglia single unit activity and spontaneous motor activity is dependent upon the presence of endogenous dopamine to stimulate D1 receptors; in rats treated with alpha-methyl-rho-tyrosine to reduce endogenous dopamine levels, the neurophysiological and behavioral effects of the D2 agonist quinpirole are significantly attenuated, while the effects of nonselective agonists like apomorphine, which stimulate both D1 and D2 receptors, or combinations of a D2 agonist and a D1 agonist are not attenuated. Thus, the previously held view that D2 receptors alone are responsible for evoking the changes in behavior and basal ganglia output induced by nonselective dopamine agonists and endogenous dopamine is not supported by these results, which indicate that these phenomena require concurrent stimulation of both dopamine receptor subtypes.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Neurochemical and behavioral evidence that Ro 41-9067 is a selective presynaptic dopamine receptor agonist.

(-)-2,3,4a,5,6,10b-Hexahydro-7-hydroxy-2-methylbenzo(f)-quinoline 4(1H)-ethanol (Ro 41-9067) was compared with apomorphine, 2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine (B-HT 920), lisuride and other dopamine (DA) receptor agonists in a series of tests designed to characterize its pharmacological activity on DA receptors. In vitro binding studies indicated that Ro 41-9067 bound selectively to DA D2 vs. D1 receptors. It also had a moderate affinity for serotonin1A and alpha-2 adrenergic receptors. Ro 41-9067 exhibited a marked agonistic component for the presynaptic DA autoreceptors. Indeed, it caused a dose-related reduction in locomotor activity over a wide dose range and prolonged periods of observation without stimulating locomotor activity, reflecting postsynaptic DA receptor activation, even at the highest doses. Ro 41-9067 inhibited the gamma-butyrolactone-induced increase in I-dopa accumulation in the rat striatum, an effect sensitive to haloperiodol. Ro 41-9067 inhibited K(+)-induced [3H]DA release and significantly reduced the striatal contents of the DA metabolites, dihydroxyphenilacetic acid and homovanillic acid. Furthermore, the compound counteracted stereotyped behavior and locomotor stimulation induced by amphetamine. Finally, Ro 41-9067 did not appear to act on postsynaptic D2 receptors because it, similarly to B-HT 920 but differently from bromocriptine, quinpirole and lisuride, did not change basal or forskolin-stimulated adenylate cyclase activity. Only at very high concentrations Ro 41-9067 increased adenylate cyclase activity, this effect being due to a D1 agonistic component.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Butyrolactone↗
PubMed1993

The NMDA positive modulator D-cycloserine potentiates the neuroleptic activity of D1 and D2 dopamine receptor blockers in the rat.

According to the view that N-methyl-D-aspartate (NMDA) agonists could be seen as putative therapeutic agents in schizophrenia, the present study was aimed at investigating whether the NMDA positive modulator D-cycloserine (DCS) could show neuroleptic activity. When given alone, DCS (1.5, 3, 6, 12 mg/kg) failed to affect the stereotyped behavior induced by 0.5 mg/kg SC apomorphine, a test routinely used to detect neuroleptic activity. Nevertheless, the administration of different doses of DCS (1.5, 3, 6 mg/kg) in combination with the D1 dopamine receptor blocker SCH 23390 or the D2 antagonist YM 09151-2, both given in doses which by themselves were ineffective in blocking apomorphine elicited behavior, induced a dose- dependent neuroleptic effect. Furthermore the positive NMDA modulator allowed (-)-sulpiride, which given alone never antagonized the apomorphine-induced stereotypy, to exhibit a full neuroleptic activity. The lower dose of DCS effective in potentiating antipsychotic effect of dopaminergic blockers also counteracted the behavioral response (hypermotility) induced by the NMDA negative modulator MK-801 (0.25 mg/kg), thus indicating the specificity of DCS effect. The results strengthen the view that drugs which increase NMDA receptor function could be a useful supplement in the therapy of psychotic disorders.

Animals↗
PubMed1988

Synthesis and dopamine agonist and antagonist effects of (R)-(-)- and (S)-(+)-11-hydroxy-N-n-propylnoraporphine.

The R-(-) and S-(+) enantiomers of 11-hydroxy-N-n-propylnoraporphine, (R)-3 and (S)-3, were synthesized in six steps from 1-(3-methoxy-2-nitrobenzyl)isoquinoline. Neuropharmacological evaluation of the R and S isomers (by affinity to dopamine receptor sites in rat brain tissues, induction of stereotyped behavior, and interaction with motor arousal induced by (R)-apomorphine in the rat) indicated that, similar to the 10,11-dihydroxy congener 2, both enantiomers can bind to dopamine receptors but that only (R)-3 activates them, whereas (S)-3 shows activity as a dopaminergic antagonist.

Animals↗
PubMed1981

Stereotypy and striatal dopamine receptor changes with 1-alpha-acetylmethadol (LAAM).

Narcotics like morphine and methadone produce effects on striatal dopaminergic mechanisms as evidenced by changes in a stereotyped behavior induced by apomorphine and binding or radioactive ligands to dopamine (DA) receptors. LAAM may replace methadone in the treatment of narcotic addiction. We investigated the effect of LAAM on apomorphine induced stereotypy and the binding of 3H-spiroperidol to dopamine receptors isolated from mouse and guinea pig striata. Chronic LAAM treatment produced a behavioral supersensitivity to apomorphine. The biochemical expression of the behavioral effect was a significant increase in the number of dopamine receptor binding sits in mouse and guinea pig striata. These effects can be due to either a direct chronic blockade or postsynaptic dopamine receptors or stimulation of a presynaptic receptor which acts to reduce the amount of dopamine released during nerve activity. Work is in progress to determine the mechanism of this effect.

Animals↗
PubMed1986

Evidence that thioridazine enhances amphetamine-induced stereotypy via anticholinergic activity.

The hypothesis that the anticholinergic properties of thioridazine can account for its ability to enhance amphetamine-induced stereotyped behaviors was tested. In one experiment, scopolamine-induced repetitive head movements were shown to be potentiated by thioridazine. In another experiment, subthreshold doses of scopolamine and thioridazine interacted to potentiate amphetamine-induced repetitive head movements. The data suggest that thioridazine, in addition to its neuroleptic activity, has significant anticholinergic effects in vivo and these effects may account for its potentiation of amphetamine-induced stereotypy.

Animals↗
PubMed1999

Kinetic analysis of GM1 effects on haloperidol-induced dopaminergic supersensitivity.

The relative affinity of metoclopramide as indicated by K(B) values was calculated in control and in haloperidol-withdrawn rats treated or not with monosialoganglioside-1 (GM1) by using dose-response curves constructed for apomorphine-induced stereotyped behavior. Haloperidol withdrawal decreased K(B) data--that is, increased the D2-receptor affinity for metoclopramide. GM1 treatment per se did not modify K(B) values but, when given in combination with haloperidol, GM1 induced a decrease in K(B) values. No differences were found in K(B) data when GM1 was administered after withdrawal from haloperidol.

Animals↗
PubMed1985

Chronobiological aspects of stereotypy.

An area of research concerned with the temporal structure of stereotypic behavior, namely, the chronobiology of stereotypy, was reviewed. Nine studies in which investigators examined the long-term temporal structure of stereotypy of mentally retarded individuals were reviewed. Seven of them indicated that stereotypy occurs in a rhythmic pattern over time. The origins of these patterns were related to both exogenous and endogenous factors, such as staff and activity changes, metabolic functions, and the existence of a rest-activity cycle.

Arousal↗
PubMed1980

Is dopamine antagonism a requisite of neuroleptic activity?

Neuroleptic activity in laboratory animals is characterized by a decrease in locomotor activity, ptosis, catalepsy, antagonism of certain amphetamine-induced responses, and inhibition of a conditioned avoidance response. Neuroleptics have also been shown to be potent antagonists of dopamine (DA), cis-5,6-Dimethoxy-2-methyl-3-[2-(4-phenyl-1-piperazinyl)-ethyl]indoline (DHO) has been shown to possess the above described pharmacological profile. However, in contrast to known neuroleptics, DHO has no effect on DA levels, DA turnover rate or DA-stimulated cyclase; nor did it have an effect on tyrosine hydroxylase activity. In addition, DHO did not antagonize apomorphine-induced gnawing or amphetamine-induced stereotyped behavior, both of which have been reported to be DA-dependent. However, the agent decreased the level of norepinephrine in the forebrain. An attempt is made to demonstrate that the "DA-hypothesis" of schizophrenia may not be valid in all cases, and that the biochemistry of the disease state is very complex.

Amphetamine↗
PubMed1981

[Neurophysiologic and pharmacologic evidence of autoregulationin the nigrostriatal system].

Repeated electrical stimulation of substantia nigra in cats produces a progressive relaxation of the poststimulation stereotyped behavior. This effect may be consequent on the development of autoinhibition in the nigro-striatal pathways since the rate of stereotypy inhibition increases in the presence of low doses of amphetamine and apomorphine but is reduced by little doses of haloperidol. A possible reason for autoinhibition is likely to involve an activation of the presynaptic dopaminergic receptors on nigro-striatal axons.

Amphetamine↗
PubMed1980

Amantadine reduces haloperidol-induced dopamine receptor hypersensitivity in the striatum.

In this report evidence is presented that amantadine hydrochloride greatly reduced the development of dopaminergic receptor hypersensitivity in the striatum, which normally results following chronic haloperidol administration using both a stereotyped behavior bioassay and a [3H]spiroperidol receptor binding assay. Amantadine prophylaxis reduced maximal ligand binding to near control levels and also significantly reduced apomorphine induced stereotypy. These results clearly demonstrate that amantadine greatly reduced haloperidol-induced striatal dopamine receptor hypersensitivity and support the hypothesis that amantadine given concurrently with neuroleptic agents might serve to prevent the development of human tardive dyskinesia.

Amantadine↗
PubMed1987

[3H]GBR 12935 binding in vivo in mouse brain: labelling of a piperazine acceptor site.

The binding of the selective dopamine uptake inhibitor [3H]GBR 12935 was studied in vivo in mouse brain. The binding was reversible with t1/2 = 80 min. The localisation of [3H]GBR 12935 binding and of dopaminergic receptors did not overlap. The binding of [3H]GBR 12935 was distributed almost uniformly throughout the brain. Also, the in vitro inhibition of dopamine uptake and the inhibition of in vivo [3H]GBR 12935 binding did not correlate when a series of relevant reference compounds was used. The potencies of various dopamine uptake inhibitors to induce stereotyped behavior did not correspond to the inhibitory potencies in the [3H]GBR 12935 binding assay. In conclusion, [3H]GBR 12935 labels in vivo a site which is different from the dopamine uptake complex. We have recently obtained results for the in vitro binding of [3H]GBR 12935 that indicate that this site could be a piperazine acceptor site.

Animals↗
PubMed2003

The significance of ear plugging in localization-related epilepsy.

PURPOSE: The localizing value of ear plugging in the treatment of auditory onset partial seizures, to our knowledge, has not been previously described. We propose that ear plugging is a clinical response to a sensory seizure manifested as an auditory hallucination and a tool for identifying the seizure focus in the auditory cortex on the superior temporal gyrus. METHODS: We report on three children who had prior epilepsy surgery for recurrent symptomatic localization-related epilepsy and who, subsequent to their surgery, displayed stereotyped unilateral or bilateral ear plugging at the onset of partial seizures. We studied scalp video electroencephalography (VEEG), magnetoencephalography (MEG), and magnetic resonance imaging (MRI) in all three. Additionally, we used electrocorticography (ECoG) in two patients, intracranial VEEG monitoring in one patient, and functional MRI language mapping in two patients. RESULTS: All three patients plugged their ears with their hands during auditory auras that localized to the superior temporal gyrus and were followed by partial seizures that spread to a wider field, as shown on scalp and intracranial VEEG. All three patients had MEG interictal discharges in the superior temporal gyrus. One patient who was nonverbal and unable to describe an auditory phenomenon plugged the ear contralateral to where temporal lobe-onset seizures and MEG interictal discharges occurred. CONCLUSIONS; Ear-plugging seizures indicate an auditory aura and may also lateralize seizure onset to the contralateral temporal lobe auditory cortex. Stereotyped behaviors accompanied by epileptic seizures in children who have poor communication skills are important in the seizure semiology of localization-related epilepsy.

Adolescent↗
PubMed1976

Blockade of apomorphine's discriminative stimulus properties: relation to neuroleptic activity in neuropharmacological and biochemical assays.

Using a food-reinforced two-lever operant conditioning procedure, rats were trained to discriminate 0.16 mg/kg apomorphine from saline. Eight neuroleptics of the phenothiazine, butyrophenone or diphenylbutylamine type were investigated for thsir ability to antagonize the discriminative stimulus properties of apomorphine. The same drugs were also assayed for in vivo antagonism of apomorphine-induced stereotyped behavior as well as for in vitro inhibition of stereospecific 3-H-haloperidol binding in rat striatal tissue preparations. The data are consistent with the hypothesis that apomorphine exerts its discriminative stimulus properties by a mechanism similar to that underlying its stereotypogenic action. The loci involved in these two phenomena are likely to be distinct.

Animals↗
PubMed1977

Synthesis and stereospecific antipsychotic activity of (-)-1-cyclopropylmethyl-4-(3-trifluoromethylthio-5H-dibenzo[a,d]cyclohepten-5-ylidene)piperidine.

The synthesis and resolution of 3-iodocyproheptadine [(+/-)-5a] and 1-cyclopropylmethyl-4-(3-iodo-5H-dibenzo-[a,d]cyclohepten-5-ylidene)piperidine [(+/-)-5b] are described. The resulting atropisomers undergo reaction with trifluoromethylthiocopper to give optically active products without extensive racemization. In this manner, optically pure (+)- and (-)-3-trifluoromethylthiocyproheptadine [(+)-6a and (-)-6a, respectively] and (+)- and (-)-1-cyclopropylmethyl-4-(3-trifluoromethylthio-5H-dibenzo[a,d]cyclohepten-5-ylidene)piperidine [(+)-6b and (-)-6b, respectively] have been prepared. The influence of a chiral europium shift reagent on the proton and fluorine resonance signals as a diagnostic tool for the determination of the optical purities of these atropisomers is discussed. The four compounds, (+)-6a, (-)-6a, (+)-6b, and (-)-6b, were studied in squirrel monkeys for their ability to block conditioned avoidance responding. All of the antiavoidance activity was found to reside solely in the levorotatory compounds (-)-6a and (-)-6b. Further comparison of the enantiomers (-)-6b and (+)-6b showed that the ability to antagonize apomorphine-induced stereotyped behavior is confined to the levorotatory isomer (-)-6b while weak central anticholinergic activity resides solely in the dextrorotatory isomer (+)-6b. Neither (-)-6b has significant peripheral anticholinergic activity.

Animals↗
PubMed2005

Tetrahydrobiopterin in the treatment of children with autistic disorder: a double-blind placebo-controlled crossover study.

Twelve children, all boys, aged 4 to 7 years, with a diagnosis of autistic disorder and low concentrations of spinal 6R-l-erythro-5,6,7,8-tetrahydrobiopterin (tetrahydrobiopterin) were selected to participate in a double-blind, randomized, placebo-controlled, crossover study. The children received a daily dose of 3 mg tetrahydrobiopterin per kilogram during 6 months alternating with placebo. Treatment-induced effects were assessed with the Childhood Autism Rating Scale every third month. The results showed small nonsignificant changes in the total scores of Childhood Autism Rating Scale after 3- and 6-month treatment. Post hoc analysis looking at the 3 core symptoms of autism, that is, social interaction, communication, and stereotyped behaviors, revealed a significant improvement of the social interaction score after 6 months of active treatment. In addition, a high positive correlation was found between response of the social interaction score and IQ. The results indicate a possible effect of tetrahydrobiopterin treatment.

Autistic Disorder↗
PubMed1988

7-[3-(4-[2,3-Dimethylphenyl]piperazinyl)propoxy]-2(1H)-quinolinone (OPC-4392), a presynaptic dopamine autoreceptor agonist and postsynaptic D2 receptor antagonist.

7-[3-(4-[2,3-dimethylphenyl]piperazinyl)propoxy]-2(1H)-quinolinone (OPC-4392), was synthesized in our laboratories and compared with apomorphine, 3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP) and dopamine antagonists in a series of tests designed to characterize dopamine receptor activation and inhibition. The assertion that OPC-4392 acts as an agonist at presynaptic dopamine autoreceptors is supported by the following behavioral and biochemical observations: OPC-4392, 3-PPP and apomorphine inhibited the reserpine-induced increase in DOPA accumulation in the forebrain of mice and in the frontal cortex, limbic forebrain and striatum of rats. In addition, the gamma-butyrolactone (GBL)-induced increase in DOPA accumulation in the mouse forebrain was also inhibited by OPC-4392, 3-PPP and apomorphine. Haloperidol antagonized the inhibitory effect of OPC-4392 in both instances. The inhibitory effect of OPC-4392 on GBL-induced DOPA accumulation lasted for at least 8 hours after oral administration to mice, while that of 3-PPP and apomorphine disappeared in 4 hours after subcutaneous injection. OPC-4392 failed to increase spontaneous motor activity in reserpinized mice, enhance spontaneous ipsilateral rotation in rats with unilateral striatal kainic acid (KA) lesions, induce contralateral rotation in rats with unilateral striatal 6-hydroxydopamine (6-OHDA) lesions and inhibit 14C-acetylcholine (Ach) release stimulated by 20 mM KCl in rat striatal slices. In addition, OPC-4392 appears to block postsynaptic D2 receptors since OPC-4392, as well as dopamine antagonists, was able to inhibit stereotyped behavior and climbing behavior induced by apomorphine in mice, displace the 3H-spiroperidol binding to rat synaptosomal membranes in vitro and reverse the inhibitory effect of apomorphine on Ach release in rat striatal slices. These results suggest that OPC-4392 acts as a dopamine agonist at presynaptic autoreceptors related to dopamine synthesis and acts as dopamine antagonist at postsynaptic D2 receptors.

Animals↗