PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Stereotyped Behavior”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 649 records · Page 36Linked to original sources
PubMed1999

Possible role of neuropeptides in obsessive compulsive disorder.

The most consistent finding in clinical research of obsessive compulsive disorder (OCD) is the significant treatment advantage of potent serotonin uptake inhibitors (SUIs) over other classes of antidepressant and antianxiety drugs. Clinical neurobiological studies of OCD, however, have yielded limited and inconsistent evidence for significant fundamental abnormalities in monoamine systems including serotonin, norepinephrine and dopamine. Furthermore, one-third to one-half of OCD patients do not experience a clinically meaningful improvement with SUI treatment. Investigation beyond the monoamine systems may be necessary in order to more fully understand the pathophysiology of obsessive-compulsive symptoms and develop improved treatments. Evidence from preclinical studies suggests that neuropeptides may have important influences on memory acquisition, maintenance and retrieval; grooming, maternal, sexual and aggressive behavior; fixed action patterns; and stereotyped behavior; these phenomena may relate to some features of OCD. In addition, extensive interactions have been identified in the brain between neuropeptidergic and monoaminergic systems, including co-localization among specific populations of neurons. The purpose of this review is to present the current knowledge of the role of neuropeptides in the clinical neurobiology of children, adolescents and adults with OCD focusing primarily on results from pharmacological challenge and cerebrospinal fluid studies. Where evidence exists, developmentally regulated differences in neuropeptide function between children and adolescents versus adults with OCD will be emphasized; these data are intended to underscore the potential importance of establishing the age of symptom onset (childhood versus adult) in individual patients with OCD participating in clinical neurobiological investigations. Likewise, where information is available, differences in measures of neuropeptides between patients with non-tic-related OCD versus tic-related OCD will be highlighted; these data will demonstrate the critical value of diagnostic precision, as these two particular subtypes of OCD may have different neurochemical underpinnings.

Adolescent↗
PubMedDate not supplied

[Sensitivity of animals to central nervous system stimulants in hypokinesia].

The experiments were carried out on 1150 non-inbred white male rats weighing 200+/-50 g. The animals were housed in small cages for 1, 5, 10, 15, 30, 45 and 60 days. Control rats remained normally active. The experimental and control animals were given a typical diet. On the above days the rats were injected intraperitoneally with central nervous stimulants--caffeine, phenamine and strychnine. Changes in the animal sensitivity to the stimulants were measured with respect to the alterating of LD16, LD50 and LD54 in test animals as compared with the controls and in regards to the emergence and duration of behavioural reactions: adynamics (caffeine), stereotype behavior (phenamine) and convulsions (strychnine). The greatest changes in the animal sensitivity were noted in response to phenamine. A significant increase in the sensitivity to caffeine was found on the 5, 15 and 45th experimental days and to strychnine only on the 5 and 45th days. Convulsions in response to strychnine were recorded in experimental animals earlier than in the controls and their duration was dependent on the doses injected. Adynamics in response to caffeine developed in experimental rats later than in the controls (on the 15th day) and its duration changed cyclically. Stereotype behavior in response to phenamine showed cyclic pattern and its duration in experimental rats was shorter than in the controls.

Amphetamine↗
PubMed2002

Subchronic caffeine administration sensitizes rats to the motor-activating effects of dopamine D(1) and D(2) receptor agonists.

RATIONALE: Dopamine transmission acting at either the D(1) or D(2) receptor level is known to influence the stimulant properties of caffeine, an antagonist of adenosine A(1) and A(2) receptors. In contrast, how caffeine influences the motor stimulant properties of selective D(1) and D(2) receptor agonists is still undefined. OBJECTIVES: In this study the acute motor response to the dopamine D(1) receptor agonist SKF 77434 and the D(2)/D(3) receptor agonist quinpirole was studied in rats treated subchronically with caffeine (15 mg/kg i.p., on alternate days) or vehicle, either in the test cage (paired group) or in the home cage (home group). METHODS AND RESULTS: Repeated caffeine administration did not induce any significant increase in motor activity or in stereotyped behavior during the course of treatment, indicating that the response to caffeine itself did not develop sensitization. Three days after the last caffeine or vehicle administration, rats were challenged with caffeine, SKF 77434, or quinpirole. Caffeine (5 mg/kg i.p.) elicited the same motor stimulant effects in both caffeine- and vehicle-pretreated rats, confirming the presence of neither tolerance nor sensitization to caffeine itself. SKF 77434 (3 mg/kg s.c.) elicited a higher locomotor activation in caffeine- than in vehicle-pretreated rats, whereas quinpirole (0.15 mg/kg s.c.) induced a similar locomotor activation and a higher stereotyped behavior in caffeine-pretreated rats as compared to rats pretreated with vehicle. The sensitized response to SKF 77434 and quinpirole was not due to environmental conditioning since the responses were similar in either paired or home group. CONCLUSIONS: The results provide support for the presence of long-term functional interactions between drugs acting at the adenosine and dopamine receptor levels. Subchronic caffeine, by sensitizing the motor stimulant effects of dopamine D(1) and D(2) receptor agonists, produces adaptive changes which might result in a potentiation of the dopaminergic component of drugs of abuse.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

SCH 23390-induced behavioral supersensitivity is not related to striatal c-fos levels.

Stereotyped behavior and striatal c-fos levels induced by chronic treatment with the D1 dopamine antagonist SCH 23390 have been investigated in rats which received subsequent subacute dopamine agonist treatment. SCH 23390 treatment (0.5 mg/kg/day) for 21 days increased both apomorphine-induced orofacial stereotypies and striatal c-fos levels. Treatment with the D1 dopamine agonist SKF 38393 (10 mg/kg/day) and the combination of SKF 38393 with the D2 dopamine agonist quinpirole (1 mg/kg/day), for 5 consecutive days, attenuated apomorphine-induced stereotypies without changing c-fos levels in rats previously treated with SCH 23390. These findings suggest that SCH 23390-induced behavioral supersensitivity and the increased striatal c-fos levels are concomitant but unrelated phenomena.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Effects of lesions of prefrontal cortex, amygdala, or fornix on behavioral sensitization to amphetamine: comparison with N-methyl-D-aspartate antagonists.

Behavioral sensitization to amphetamine involves the mesoaccumbens dopamine system and is accompanied by cellular changes in this system. Excitatory amino acid antagonists, when co-administered with amphetamine, prevent both behavioral sensitization and associated changes in the mesoaccumbens dopamine system. This suggests that excitatory amino acid-dependent events are critical to the initiation of sensitization. This study sought to identify excitatory amino acid projections required for sensitization, focusing on projections to the nucleus accumbens or ventral tegmental area. The major excitatory projections to the nucleus accumbens originate in the prefrontal cortex, amygdala and hippocampus. The prefrontal cortex and amygdala also send excitatory projections to the ventral tegmental area. Ibotenic acid lesions of the prefrontal cortex or amygdala and electrolytic lesions of the fornix were performed in rats. After one week of recovery, rats were treated with water or 2.5 mg/kg amphetamine for six days and challenged with amphetamine on day 8. Activity was tested in photobeam cages on days 1 and 8. On day 1, control and sham-lesioned rats exhibited stereotyped behaviors followed by a period of post-stereotypy locomotion. On day 8, sensitization was evident as an enhancement of both stereotypy and post-stereotypy locomotion. Co-administration of N-methyl-D-aspartate antagonists [MK-801 (dizocilpine maleate) or CGS 19755] with amphetamine prevented the development of sensitization of both stereotypy and post-stereotypy locomotion. Neither antagonist, however, prevented the expression of sensitization. None of the lesions completely mimicked these effects of N-methyl-D-aspartate antagonists. Lesions of hippocampal projections traveling in the fornix produced a general disinhibition of locomotor activity, but did not prevent sensitization of either stereotypy or post-stereotypy locomotion. Lesions of the prefrontal cortex failed to prevent sensitization of stereotypy was obtained following repeated amphetamine administration. However, like prefrontal cortical lesions, amygdala lesions prevented sensitization of post-stereotypy locomotion. When interpreted in the light of previous studies demonstrating the importance of the ventral tegmental area in the initiation of sensitization, the present results suggest a likely role for neuronal circuits involving the prefrontal cortex, amygdala and ventral tegmental area in the development of sensitization of post-stereotypy locomotion following repeated amphetamine administration. Such circuits may initiate sensitization through a mechanism involving excitatory amino acid regulation of the activity of mesoaccumbens dopamine neurons. Parallel circuits, involving other brain regions, may similarly contribute to sensitization of stereotyped behaviors.

Amphetamine↗
PubMed1983

gamma-Butyrolactone effects on behavior induced by dopamine agonists.

gamma-Butyrolactone (GBL) potently inhibits stereotyped behavior induced by indirect (amphetamine and methylphenidate) and direct (apomorphine) dopamine agonists. Amphetamine induces a dose-response partial reversal of the GBL effect. The GABA antagonist, bicuculline, only partially reverses the GBL inhibition of apomorphine activity, indicating that GBL may be acting through mechanisms in addition to effects on GABA.

4-Butyrolactone↗
PubMed1986

Disposition of apomorphine in rat brain areas: relationship to stereotypy.

Apomorphine-induced stereotyped behavior and apomorphine levels in plasma, striatum and nucleus accumbens were determined in rats at various intervals after a single i.p. injection of serial doses of apomorphine hydrochloride (0.625, 1.25, 2.5 and 5 mg/kg). Apomorphine disappeared from plasma in a mono-exponential mode with a half-life of about 10 min. In striatum and nucleus accumbens apomorphine concentrations peaked 10 min after administration, declining thereafter with a half-life comparable to that in plasma. Apomorphine was concentrated and distributed similarly in the two brain regions; the brain areas/plasma ratio was approximately seven for all doses tested. The rise of apomorphine levels in brain areas slightly preceded the behavioral response, whereas after the peak effect (20-30 min) the intensity of stereotypy declined almost parallel with the log drug concentrations. Plotting apomorphine levels in the tissues assayed against the drug response at the same interval for individual rats, regardless of dose, indicated a highly significant relation between the degree of behavioral effects and brain apomorphine levels. The threshold apomorphine concentrations for inducing stereotyped behaviour were 108 and 95 ng/g respectively in striatum and nucleus accumbens. These findings show that the time course and magnitude of the behavioral effects of apomorphine corresponded with its brain levels in 'dopaminergic' areas, suggesting that apomorphine-induced stereotyped behavior in rats can be described by a direct mechanism. Reserpine (5 mg/kg s.c.) enhanced the apomorphine stereotypy but did not affect apomorphine's disposition in brain and plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Repeated cocaine administration increases GABA(B(1)) subunit mRNA in rat brain.

The effects of a single and repeated administration of cocaine on GABA(B) receptor subunit mRNA was investigated in rat brain by in situ hybridization. Following a single administration of cocaine, no significant change was observed in any brain regions examined, neither 1 h nor 24 h after administration. During repeated administration of cocaine, behavioral sensitization with increased stereotyped behavior was observed. A significant increase in the level of GABA(B(1)) mRNA was observed in the nucleus accumbens (11.4%), CA1 field of the hippocampus (16.8%), and thalamus (16.5%) 1 day after repeated administrations of cocaine for 14 consecutive days. The level of mRNA returned to the basal level 1 week after the final injection of repeated cocaine treatment. The observed changes in the mRNA level after the repeated cocaine may imply changes of GABA(B(1)) subunit in molecular mechanisms which underlie development of behavioral sensitization.

Animals↗
PubMed2003

Postsynaptic dopamine (D(2))-mediated behavioural effects of high acute doses of artemisinin in rodents.

Artemisinin or qinghaosu is the active principle of quinghao (Artemisia annua L.) developed from Chinese traditional medicine, which is now widely used around the world against falciparum malaria. Behavioural effects of high acute doses of artemisinin were studied on spontaneous motor activity (SMA), exploratory behavior, apomorphine-induced stereotype behavior and pentobarbital sleeping time in mice and rats in order to provide additional evidence on its safety profile on the central nervous system (CNS). Effects of the drug on bromocriptine-induced hyperactivity in short term reserpinised mice were also evaluated. Intraperitoneal (i.p.) injection of artemisinin at doses of 50 and 100mg/kg, significantly (P<0.05) reduced the SMA in mice, prolonged the pentobarbital sleeping time in rats, and attenuated the apomorphine-induced stereotypy in mice. Mice pretreated with reserpine, showed a significant decrease in locomotor activity compared to the saline-treated group. Bromocriptine, a D(2) receptor agonist, induced locomotor activity in mice pretreated with reserpine which was attenuated by artemisinin. The results suggest that artemisinin possesses sedative property, which may be mediated via postsynaptic dopamine (D(2)) receptor in the CNS.

Animals↗
PubMed1999

Molecular cloning and biological activity of ecdysis-triggering hormones in Drosophila melanogaster.

Ecdysis-triggering hormones (ETH) initiate a defined behavioral sequence leading to shedding of the insect cuticle. We have identified eth, a gene encoding peptides with ETH-like structure and biological activity in Drosophila melanogaster. The open reading frame contains three putative peptides based on canonical endopeptidase cleavage and amidation sites. Two of the predicted peptides (DrmETH1 and DrmETH2) prepared by chemical synthesis induce premature eclosion upon injection into pharate adults. The promoter region of the gene contains a direct repeat ecdysteroid response element. Identification of eth in Drosophila provides opportunities for genetic manipulation of endocrine and behavioral events underlying a stereotypic behavior.

Amino Acid Sequence↗
PubMed1987

Clinical features of autistic children with setback course in their infancy.

This study examines the incidence rate of setback in 80 autistic children, the correlation between the type of onset and clinical features, developmental level and prognosis based on an originally developed questionnaire. Moreover, this study seeks to investigate the possibility that infantile autism might be classified into subgroups by the type of onset. 1) The acquired (including questionably acquired) group consisted of 39 cases (49%), while the natal group was made up of 41 cases (51%). 2) The age when the setback occurred was 21-22 months in the acquired group. 3) Precipitating psychological events were observed in 22 cases (56%) of the acquired group. 4) The mental developmental level including speech and socialbility function at 5 years of age was significantly lower in the acquired group than in the natal group. 5) The acquired group showed severe behavioral disorders such as "stereotypic behavior," "extremely hyperkinetic behavior" and "self-abusive behavior" compared with the natal group. 6) The adaptive levels at schools or institutions were lower in the acquired group than in the natal group. 7) There was a higher incidence of epileptic seizures or febrile convulsions in the acquired group than in the natal group. Moreover, there was a higher incidence of severe perinatal abnormalities in the acquired group. 8) The above-mentioned results suggest that infantile autism might be classified into two subgroups, acquired and natal groups, based on the type of onset, and also suggest that some types of brain dysfunctions are more severe in the acquired group than in the natal group.

Age Factors↗
PubMed1976

MIF, TRH, and simian social and motor behavior.

MSH-release-inhibiting factor (MIF) and thyrotropin-releasing hormone (TRH) both have been reported to modify mood and activity in man. These two hypothalamic peptides were given intramuscularly across a 1000-fold dose range to 5 juvenile male M. nemestrina monkeys living in a social group. Motor activity was recorded automatically, and an observer counted various social behaviors. MIF increased motor activity for up to 11 hr. It decreased quiet foraging behavior, but did not change behaviors of social interaction. TRH did not stimulate motor behavior; high doses strongly suppressed it and produced apparent somatic distress. TRH increased behaviors of quiet rest and association and decreased environment exploration and low-intensity dominance behaviors. The lowest dose of TRH increased social play. Two monkeys showed repetitive, stereotyped behaviors even in baseline observations, and certain doses of TRH and MIF may have increased the frequency of these behaviors.

Animals↗
PubMed1983

The role of dopaminergic receptors in the behavioral effects induced by lisuride in male rats.

Lisuride increased the incidence of stretching and yawning (SY) as well as of penile erection (PE) and elicited stereotyped behavior (SB), aggressive behavior and mounting in male rats, depending on the dose used. SY was prevented by two dopaminergic antagonists, haloperidol and sulpiride, but not by methysergide, a serotoninergic antagonist, while PE was antagonized by all three drugs. With regard to SB, aggressive behavior and mounting, all three were suppressed by haloperidol; sulpiride, while partially antagonizing aggressiveness, failed to affect SB and mounting; methysergide did not significantly influence any of the three. This suggests that lisuride principally affects the dopaminergic system. Although further detailed studies are required to elucidate which type of the complex population of DA-receptors is involved in each kind of behavior, we suggest that SY at least is due to the activation by lisuride of presynaptic DA-receptors.

Aggression↗
PubMed1995

Does dizocilpine (MK-801) selectively block the enhanced responsiveness to repeated amphetamine administration?

In order to examine the hypothesis that N-methyl-D-aspartate (NMDA) receptors are selectively involved in the development of stimulant sensitization, we characterized the interaction between acute and chronic dizocilpine (MK-801) + amphetamine using a detailed behavioral analysis, including concurrent assessment of the locomotor and stereotype components of the stimulant response and continuous monitoring of all the various phases of the emergent sensitization. The results showed that MK-801 (0.125 mg/kg) significantly affected the acute response to amphetamine (0.5, 1.75, 4.0 mg/kg), increasing or decreasing locomotor activity depending on dose. Repeated administration of MK-801 + amphetamine resulted in a suppression of stereotyped behaviors and a potentiated locomotor sensitization. These findings suggest that rather than blocking the development of sensitization, MK-801 pretreatment may produce a unique behavioral augmentation that is apparent during coadministration and that persists up to 48 hr in the response to amphetamine challenge.

Amphetamine↗
PubMed1988

Neuroleptic-induced reduction of quipazine-elicited head-twitches in rats: possible involvement of striatal dopaminergic supersensitivity.

Rats were treated with a single large dose of various neuroleptic compounds and, 5-7 days after, they were assayed for either behavioral sensitivity to apomorphine (hypermotility and stereotyped behavior) or head-twitch response to the mixed serotonin-dopamine agonist quipazine. The animals withdrawn from chlorpromazine, fluphenazine, haloperidol, metoclopramide and the D1 selective blocker SCH 23390, showed enhanced hypermotility and/or stereotyped responses to apomorphine and reduced head-twitch response to quipazine. The rats withdrawn from thioridazine, (-)-sulpiride and sultopride responded to apomorphine only with enhanced hypermotility while their response to quipazine was either unchanged or even increased. The results are discussed in terms of dopaminergic brain areas and/or receptor subtypes involved in the modulation of the head-twitch response to quipazine. We concluded that an enhancement of dopaminergic tone at the striatal level could be related to the reduced head-twitch response to quipazine.

Animals↗