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Results for “Stereotyped Behavior”

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At least 487 records · Page 27Linked to original sources

PubMed1986

Potentiation of phencyclidine-induced dopamine-dependent behaviors in rats after pretreatments with serotonin-depletors.

This study was designed to assess whether phencyclidine (PCP) produces dopamine (DA)-dependent behaviors such as licking, gnawing and biting (which are not observed in normal rats) in rats after pretreatments with a tryptophan hydroxylase inhibitor, p-chlorophenylalanine (PCPA) and specific serotonergic neuronal toxin, p-chloroamphetamine (PCA). Apomorphine (APO, 0.5 mg/kg) and methamphetamine (MAP, 2.5 mg/kg) mainly induced DA-dependent behaviors, including rearing and sniffing with occasional licking, in the vehicle-pretreated rats. APO (0.5 mg/kg)-induced DA-dependent behaviors significantly increased in the PCA- and PCPA-pretreated rats, in which serotonergic activity was greatly depressed but dopaminergic activity was normal. MAP (2.5 mg/kg)-induced DA-dependent behaviors were also significantly increased in the PCA-pretreated rats but not PCPA-pretreated rats. On the other hand, at doses of 2.5-7.5 mg/kg, PCP mainly caused stereotyped behaviors such as head-weaving, backpedalling, turning and DA-dependent behavior, such as sniffing, in the vehicle-pretreated rats. The PCP-induced stereotyped behaviors were attenuated by pretreatment with PCA and PCPA. In contrast, PCP-induced DA-dependent behavior, sniffing, was converted into more intense behaviors such as licking, gnawing and biting by pretreatment with PCA. These effects of PCP were also observed in rats pretreated with PCPA, although the degree was less than that by pretreatment with PCA. These results may indicate that serotonergic neuronal systems inhibitory regulate dopaminergic systems in PCP-induced behavioral responses.

Animals↗

PubMed1983

Methamphetamine-induced behavioral effects and releases of brain catecholamines and brain concentrations of methamphetamine in mice.

The characteristic behavioral effect of methamphetamine (MA) at 2.5 mg/kg was enhanced locomotor activity which lasted over 2.5 hr. At 10.0 mg/kg MA, stereotyped behavior was predominant and lasted over 3 hr. The behavioral effect of 5.0 mg/kg MA was of the mixed type. MA at 5.0 and 10.0 mg/kg lowered the brain NE level from 2 hr after drug treatment, while the accumulation of MHPG-SO4 was increased over 2 hr at 2.5 and 5.0 mg/kg MA. The accumulation of HVA was significantly increased at 10.0 mg/kg MA over 3 hr. Accordingly, the behavioral effects of MA at the earlier period were compatible with the biochemical effects of MA. The behavioral effects during the 2- to 4-hr period, however, seem to be unrelated to the actions on brain catecholamines. Measurement of brain MA concentrations revealed that approx. 2 micrograms/g in the brain may be necessary to produce enhanced locomotor activity and the increased accumulation of brain MHPG-SO4. It appeared that approx. 8 to 9 micrograms/g MA in the brain was required to produce characteristic stereotyped behavior and the increased accumulation of HVA. Therefore, the behavioral and biochemical effects of MA were correlated with the brain MA concentrations.

Amphetamine↗

PubMed1987

A dietary haloperidol regimen for inducing dopamine receptor supersensitivity in rats.

The induction of dopaminergic supersensitivity in rats by the administration of haloperidol in their diet for 30 days (CHAL) in three increasing concentrations (7-15 mg/kg/day) was compared to that induced by single daily subcutaneous injections (SCHAL, 0.7 mg/kg) on the basis of biochemical (radioimmunoassay of serum haloperidol levels, 3H-spiroperidol binding) or behavioral (apomorphine stereotypy, spontaneous locomotor activity) parameters. The two modes of administration produced equivalent blood levels of haloperidol by day 30. At 48 hours post treatment: spontaneous locomotor activity and stereotyped behavior were significantly increased in both groups of haloperidol-treated rats, stereotyped behavior was significantly greater in CHAL- vs. SCHAL-treated rats at 8 days post treatment and specific 3H-spiroperidol binding was increased 64% and 236% within the striatum and GP, respectively, of CHAL-treated vs. control rats. Scatchard analysis of 3H-spiroperidol binding isotherms revealed a significant increase in the Bmax of high affinity binding sites [KD approximately 55 pM] within the striatum of both CHAL- and SCHAL-treated rats at 48 hours post treatment. A second, lower affinity site was resolved within the SCHAL-treated group which was not detected within striatal homogenates of CHAL-treated or control rats.

Administration, Oral↗

PubMed1982

Differential enhancement of behavioral sensitivity to apomorphine following chronic treatment of rats with (-)-sulpiride and haloperidol.

Rat exploratory activity as well as apomorphine-induced hypermotility and stereotyped behavior were assayed following acute (60 min before) or chronic (21 days) administration of sulpiride stereoisomers and haloperidol. Parallel groups of rats were assayed for their hypermotility and stereotyped responses to challenging doses of apomorphine 7 and 21 days after discontinuation of chronic treatments. Following its acute administration, (-)-sulpiride fully antagonized apomorphine-induced hypermotility without affecting the level of animal spontaneous activity and partially counteracted stereotyped behavior. Haloperidol completely suppressed both apomorphine responses and also depressed exploratory activity. Some tolerance to the anti-apomorphine effect of (-)-sulpiride groups exhibited enhanced behavioral sensitivity to apomorphine only with respect to hypermotility, whereas haloperidol groups were supersensitive with respect to both hypermotility and stereotyped responses. The results are discussed in terms of differential dopamine receptor supersensitivity arising from prolonged administration of butyrophenone and substituted benzamide.

Animals↗

PubMed2000

A component analysis of "stereotypy as reinforcement" for alternative behavior.

Results from several studies have suggested that the opportunity to engage in stereotypic behavior may function as reinforcement for alternative, more socially desirable behaviors. However, the procedural components of this intervention include several distinct operations whose effects have not been analyzed separately. While measuring the occurrence of stereotypy and an alternative behavior (manipulation of leisure materials), we exposed 3 participants to three or four components of a "stereotypy as reinforcement" contingency: (a) continuous access to materials, (b) prompts to manipulate materials, (c) restricted access to stereotypy (i.e., response blocking), and (d) access to stereotypy contingent on manipulating the materials. Continuous access to materials and prompting (a and b) produced negligible results. Restriction of stereotypy (c) produced a large increase in the alternative behavior of 2 participants, suggesting that response restriction per se may occasion alternative behavior. However, contingent access to stereotypy (d) was necessary to increase the 3rd participant's object manipulation; this finding provided some support for the use of stereotypy as reinforcement for alternative behavior. Finally, when transfer of the effects of intervention was assessed during periods in which active intervention components were withdrawn, the alternative behavior was maintained for 1 participant.

Adult↗

PubMed1994

The effect of haloperidol and naloxone on excessive grooming behavior of cats.

In a double-blind cross-over study the effect of a single injection of naloxone (1 mg/kg s.c.) was investigated in 12 cats which suffered from excessive grooming with subsequent coat damage. Based on clinical observations and reports of the owners, naloxone had a beneficial effect on grooming which lasted between 2.5 weeks and 6 months (median 3 months). In another double-blind placebo-controlled study the effect of a single injection of haloperidol (2 mg/kg i.v.) was investigated in 20 cats with excessive grooming. Within 24 h haloperidol significantly reduced the time spent grooming. Four months after the injection no effect remained in nine of 10 cats injected with a placebo solution, whereas six of 10 cats injected with haloperidol the improved condition of the coat was maintained. It is hypothesized that naloxone is only effective in counteracting recently developed stereotypic behaviors and that haloperidol rather reduces stereotyped behaviors over a longer period.

Alopecia↗

PubMed1984

In vivo electrochemical and behavioral evidence for specific neural substrates modulated differentially by enkephalin in rat stimulant stereotypy and locomotion.

The enkephalinamide, D-Ala2-D-Pro5-enkephalinamide monoacetate (WY 42, 186), when systemically administered to male Sprague-Dawley rats, significantly inhibited sniffing, repetitive head movements, and frequency of rearing, stereotyped behaviors which are often associated with nigrostriatal dopamine activation. On the other hand, the locomotor component of amphetamine-induced stereotyped behavior, which is associated with mesolimbic dopaminergic activation, was not inhibited. In vivo electrochemical analysis showed a significant decrease in striatal dopamine release from striatum after systemic administration of D-Ala2-D-Pro5-enkephalinamide monoacetate in chloral hydrate anesthetized rats, whereas the dopamine signal from the nucleus accumbens, a mesolimbic neuroanatomigic modulation of dopamine both behaviorally and biochemically. Also, the concept of separate neural systems for the stereotypic and locomotor components of amphetamine-induced stereotypy is reinforced.

Animals↗

PubMed1983

Evidence that the nigrotegmental GABAergic projection mediates stereotypy induced by apomorphine and intranigral muscimol.

The substantia nigra plays a pivotal role in the relay of output from the striatum. One neural pathway from substantia nigra projects GABAergic fibers to the caudal mesencephalic tegmentum, terminating in the vicinity of the pedunculopontine nucleus (PPN). To evaluate the functional importance of this projection in the mediation of stereotyped behaviors of striatal and nigral origin, we microinjected low doses of the GABA agonist, muscimol, bilaterally into the vicinity of the PPN. This muscimol treatment resulted in a total blockade of all stereotyped behaviors normally elicited by systemic apomorphine or by intranigral muscimol. Blockade was not observed in animals microinjected with muscimol into the dorsal reticular formation, 1 mm above the level of the PPN. Our results indicate that the nigrotegmental projection may play a crucial role in the expression of stereotyped and dyskinetic behaviors of basal ganglia origin.

Animals↗

PubMed1986

Methamphetamine-induced behavioral alterations following repeated administration of methamphetamine.

Repeated administration of a large dose of methamphetamine (MA) (25 mg/kg, i.p. twice daily for 4 days) to mice enhanced locomotor activity and decreased stereotyped behavior following a subsequent injection of MA. Simultaneous determinations of catecholamines revealed a depletion of brain dopamine. The moderate doses of haloperidol significantly enhanced MA-induced locomotor activity in mice. A significant enhancement of MA-induced locomotor activity was observed in the rats pretreated with 6-hydroxydopamine into the striatum, and this effect correlated negatively with the striatal dopamine level. These results suggest that hypofunction of striatal dopaminergic neuron systems induced by repeated administration of MA may be one of possible mechanisms of the enhancement of MA-induced locomotor activity due to the decrease of stereotyped behavior.

Animals↗

PubMed1995

[Behavioral effects of chronic apomorphine, and D-1/D-2 dopamine receptor activities in rats].

The present study was conducted to investigate the effects of chronic treatment with apomorphine on yawning and stereotyped behaviors induced by apomorphine, and catalepic responses induced by haloperidol. Rats received apomorphine (1 mg/kg, sc), a direct dopamine D1/D2 agonist, or vehicle once a day for 21 days. The chronic treatment with apomorphine shifted to the right the dose response curve of yawning to administration of apomorphine, which preferentially activates presynaptic dopamine D-2 receptors (auto receptors) at low doses. Haloperidol (0.5 mg/kg, ip)-induced catalepsy mediated by the inhibition of postsynaptic D-2 receptors was unaltered. A subsequent challenge dose of apomorphine (5 mg/kg, ip) produced oral stereotyped behaviors such as sniffing, licking and biting in the vehicle-treated rats. Chronic apomorphine treatment produced significant enhancement of sniffing alone, which may be behavioral sensitization to apomorphine, and, in contrast, attenuated licking and biting, which depend on D-2 receptor activities. These phenomena lasted for at least 30 days. Sniffing might involve relatively increased stimulation of D-1 receptors, as compared with licking and biting. These results suggest that chronic apomorphine reduces presynaptic dopamine D-2 receptor activity, and as a consequence may induce long-lasting postsynaptic dopamine receptor (mainly D-1 receptor) activation.

Animals↗

PubMed1995

Amphetamine levels in brain microdialysate, caudate/putamen, substantia nigra and plasma after dosage that produces either behavioral or neurotoxic effects.

Extracellular levels of d-amphetamine (AMPH) in caudate/putamen were determined using microdialysis and HPLC quantitation after s.c. doses that produced increased motor activity (1 mg/kg), stereotypic behavior (2.5 mg/kg) or dopamine depletion in the caudate/putamen (4 x 5 mg/kg). In 6-mo-old rats exposed to neurotoxic doses of AMPH sulfate (4 x 5 mg/kg in a 23 degrees C environment), extracellular caudate/putamen AMPH rose to levels of 7.9 +/- 0.9 microM after the first dose and peaked at 15.1 +/- 2.5 microM after the third dose with no further increases after the fourth dose. After one or three doses of 5 mg/kg, peak plasma and tissue levels of AMPH were 1.7 +/- 0.2 and 2.9 +/- 0.3 microM in plasma, 36 +/- 6 and 73 +/- 10 in substantia nigra and 25 +/- 4 and 50 +/- 8 in caudate/putamen, respectively. Caudate/putamen extracellular AMPH levels were about three times higher (in either 6- or 12-mo-old rats) after 4 x 15 mg/kg in a 10 degrees C environment and tissue levels in caudate/putamen and substantia nigra were three to five times higher after three doses of AMPH. However, these higher levels did not produce dopamine depletion in the caudate/putamen, while the lower doses (4 x 5 mg/kg) given at 23 degrees C did. Estimated caudate/putamen extracellular AMPH levels of 2.5 to 5 microM after single doses (1 and 2.5 mg/kg) that caused hyperactivity and stereotypic behavior are compatible with the 2 to 10 microM AMPH concentrations reported to be necessary to produce pronounced dopamine release in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Atropine stereotypy and its inhibition by intracaudate triperidol in the rat.

One component (rearing) of the stereotyped behavior of the rat was quantitated using erigometer, a new device developed in this laboratory. Intraperitoneal injection of atropine, but not methylatropine, caused dose-related stereotyped behavior in the rat and this effect was antagonized by intracaudate injection of triperidol in a dose-related manner. It is concluded that stereotypy can be evoked also in the case when the striatal dopaminergic tone is normal or even below normal: it is the equilibrium of the striatal cholinergic-dopaminergic systems which must be shifted towards dopamine, which is necessary for the development of this behavioral manifestation.

Animals↗

PubMed1991

MK-801 attenuates the dopamine-releasing but not the behavioral effects of methamphetamine: an in vivo microdialysis study.

Neuroanatomical and pharmacological evidence suggests that important modulatory relationships exist between mesostriatal dopaminergic terminals and corticostriatal inputs. The present study used in vivo microdialysis in awake animals to examine the results of pharmacological manipulations of these systems on net striatal dopamine (DA) efflux and behavioral activation. A single methamphetamine (m-AMPH) treatment induced a prolonged (greater than 6 h) increase (6-fold peak response) in extracellular striatal DA and increased stereotypic behavior. When given alone, the non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801 did not have a significant effect on extracellular striatal DA, but significantly increased stereotypic behaviors. Pretreatment with MK-801 markedly attenuated the m-AMPH-induced striatal DA overflow. In contrast to its effects on striatal DA overflow, MK-801 potentiated the locomotor effects of m-AMPH without reducing stereotypy rating scores. These findings suggest that the synaptic relationships between mesostriatal DA and corticostriatal excitatory amino acid terminals in the striatum are an important component in its behavioral output. Moreover, NMDA receptors appear to be capable of modulating striatal DA overflow.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

Biochemical and behavioral changes in rats during and after chronic d-amphetamine exposure.

Two groups of rats were implanted with ALZET minipumps to deliver vehicle or a theoretical amount of 1 mg/kg per h of d-amphetamine (A) for 12 days. After 3 days of A-exposure, motor movements and stereotypic behavior were markedly increased. Subsequent testing during A-exposure showed that motor movements and stereotypic behavior remained significantly increased but declined. After removal of the pumps, these effects disappeared and no differences at rest, during stress or A challenge, were apparent in either group. Animals sacrificed after 3 days of drug exposure, showed a drastic decrease in cardiac, but not adrenal, catecholamine levels. In the brain, norepinephrine (NE) levels were markedly decreased in the frontal cortex, hypothalamus, caudate, pons-medulla and cerebellum. Epinephrine (E) levels were unaffected and dopamine (DA) levels were decreased in most areas without reaching statistical significance. Plasma corticosterone levels were similar in both groups. Animals in both groups sacrificed about 25 days after pump removal were biochemically similar. Under our conditions, A-exposure produced marked behavioral and biochemical changes but there was no evidence of residual abnormalities after cessation of drug treatment.

Animals↗

PubMed1991

An automated method for the assessment of spontaneous and stereotyped climbing behavior in mice. Effects of the selective D1- and D2-dopamine receptor agonists SKF-38393 and RU-24926 and their association.

A video-tracking technique has been used for the evaluation of climbing behavior in mice. An automated image analysis system, the Videotrack 512 (Electronique Lyonnaise), was adapted for this specific application. This allowed distinguishing between spontaneous climbing and stereotyped climbing. The activity duration of mice was simultaneously measured. In order to validate this method, in the present study the ability of apomorphine to induce climbing in mice, and the effects of the D1-dopamine receptor agonist SKF-38393 and the D2-dopamine agonist RU-24926 and their association were investigated.

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

PubMed1991

Effects of methamphetamine on copulatory behavior in male rats.

Many papers have reported the effect of amphetamine and its close relative, methamphetamine on sexual activity in humans. The effect of these drugs on animal sexual behavior is unknown. The present study was done to determine whether methamphetamine modifies the copulatory behavior of male rats. Sexually experienced rats of the Wistar-Imamichi strain, 10 weeks of age, were singly injected intraperitoneally with methamphetamine hydrochloride at doses of 0, 1, 2 or 4 mg/kg body weight. Tests were initiated at 19: 30 in the dark period. Observations were conducted for 90 min. At dosages of 1 or 2 mg/kg there were no changes in copulatory behavior ascribed to the administration of methamphetamine. At 4 mg/kg the frequencies of mounting, intromission and ejaculation were greatly decreased but the spontaneous motor activity and stereotypic behavior increased in all males. In a further experiment, males were given methamphetamine by intraperitoneal injection once a week for 8 weeks. The copulatory behavior was tested 5 times at two weeks intervals. In the 4th testing, the percentage showing ejaculation decreased. In the 5th testing, there was no ejaculation and the incidence of intromission decreased. No stereotypic behavior was displayed in any of the males during the testing. From these results, it was concluded that methamphetamine inhibits the intromitting and ejaculating behavior in male rats.

Animals↗

PubMed2005

Superimposition and withholding of edible consequences as treatment for automatically reinforced stereotypy.

The delivery and subsequent withholding of tangible consequences has been previously investigated as an intervention for stereotypic behavior. The current investigation sought to extend previous research by evaluating its effectiveness and durability as treatment for stereotypy of 2 children who had been diagnosed with autism. Nonsocial functions for stereotypic behavior were identified via functional analysis. Edible items were then delivered contingent on stereotypy and were withheld in a subsequent condition. When the superimposition procedure failed to reduce stereotypy, environmental enrichment was implemented and was found to reduce the stereotypy of both participants.

Autistic Disorder↗

PubMed1984

Enhancement of behavioral effect and acute toxicity of methamphetamine by quinine in rats.

The behavioral effect and acute toxicity of methamphetamine were tested alone and in combination with quinine in rats. Quinine prolonged and increased the effect of methamphetamine. The enhancement of methamphetamine-induced stereotyped behavior was very marked when quinine was given prior to or simultaneously with methamphetamine. However, the time for onset of methamphetamine-induced stereotyped behavior was not affected by quinine. The mortality of methamphetamine was also potentiated markedly by quinine. The enhancement of the behavioral effect and the toxicity of methamphetamine may be due to inhibition of the metabolism of methamphetamine by quinine.

Animals↗