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PubMed1995

Methamphetamine-induced dopaminergic hyperactivity is not accompanied with increase in tyrosine hydroxylase mRNA of the rat midbrain.

Tyrosine hydroxylase (TH) mRNA was measured in the midbrain of rats treated repeatedly with methamphetamine (MAP). Male Sprague-Dawley rats were daily injected with MAP (5 mg/kg, i.p., once daily) or saline for 14 days. Progressive augmentation was observed in MAP-induced stereotyped behaviors. After one week of abstinence, the rats were decapitated and the brains were prepared for either in situ hybridization using non-radioactive cRNA probes or Northern blot analysis using 32P-labeled cDNA probes. In situ hybridization showed that the signals of TH mRNA were localized to the dopaminergic perikarya in the midbrain and were reduced in MAP-treated animals compared to the controls. Northern blot analysis revealed that the level of TH mRNA in the midbrain of MAP-treated rats was decreased by 37% compared to the controls, which was close to the statistical significance (P = 0.053). These results indicate that the dopaminergic hyperactivity caused by repeated MAP treatment is not associated with enhanced transcription of the TH gene.

Animals↗
PubMed1997

Locomotion and stereotypy induced by scopolamine: contributions of muscarinic receptors near the pedunculopontine tegmental nucleus.

In this study, we test whether blockade of muscarinic receptors near mesopontine cholinergic cell groups may contribute to locomotor activation induced by scopolamine. Unilateral or bilateral injections of scopolamine (10-150 micrograms) into the pedunculopontine tegmental nucleus (PPT) increased horizontal locomotion by 2-15 times in a dose-related way. Unilateral or bilateral injections of scopolamine into the PPT increased stereotypic behaviors (such as sniffing in one location or over large areas), self-biting and grooming. Carbachol (4 micrograms) injected into PPT reduced locomotion for 20 min, followed by 70 min of increased locomotion. When carbachol (4 micrograms) was injected into the PPT before scopolamine (3 mg/kg, i.p.), the activating effect of scopolamine was attenuated, but not when carbachol was injected after scopolamine. Therefore, carbachol appears to compete with scopolamine for muscarinic receptors near the PPT that mediate locomotor activating effects of systemic scopolamine. Haloperidol (0.1 mg/kg, i.p.) also attenuated the stereotypy and locomotion induced by scopolamine in the PPT. We hypothesize that scopolamine acts by blocking muscarinic receptors on mesopontine cholinergic neurons, thereby disinhibiting cholinergic neurons that can activate dopamine neurons.

Animals↗
PubMedDate not supplied

Classification of neuroleptics: implications for tardive dyskinesia.

The dopamine (DA) receptor blocking effect of neuroleptics is believed to be responsible for their antipsychotic effect. This blockade can be demonstrated in experimental animals by the ability of neuroleptics to antagonize stereotypies induced by DA agonists. Biochemically DA receptor-blocking properties of neuroleptics are illustrated by direct binding to DA receptors or by measuring inhibition of DA-stimulated adenylate cyclase activity. Most pharmacological and biochemical experiments with neuroleptics have concentrated on dopaminergic effects of the compounds both after acute and long-term treatment. After long-term treatment with neuroleptics an increase in DA receptor number and an increase in stereotyped behavior are seen. DA supersensitivity have been implied in the development of tardive dyskinesia (TD) in patients on long-term neuroleptic medication. In search for neuroleptics which would be less prone to induce TD and more effective in treating dyskinesia we have looked at the profile of a series of neuroleptics in in vitro experiments and in acute and long-term in vivo experiments. Since neuroleptics also influence other transmitter systems than the dopaminergic we have investigated interactions with drugs affecting these transmitter systems. According to their differential effects on DA receptors (D1 and D2) and their ability to develop tolerance and supersensitivity, the neuroleptics can be classified into different groups, some of which might be expected to induce less TD and be preferred for treating dyskinesia.

Animals↗
PubMedDate not supplied

Dopaminergic transmission in the rat striatum in vivo in conditions of pharmacological modulation.

The effects of pharmacological modulation of striatal dopaminergic neurotransmission were studied in freely mobile rats by intracerebral microdialysis and HPLC to assay dopamine and dopamine metabolite levels and the rate of dopamine synthesis, in combination with observations of stereotypical behavior. Inhibition of catechol O-methyltransferase (COMT) with tolcapone led to increases in extracellular dopamine levels only when the baseline dopamine level was elevated by administration of L-3,4-dihydroxyphenylalanine in combination with the decarboxylation inhibitor carbidopa. Increases in dopamine levels in striatal dialysates by blockade of reuptake were enhanced by inhibition of metabolic degradation of dopamine by tolcapone, a selective catechol O-methyltransferase inhibitor. GBR-12909, a blocker of the dopamine transporter, increased extracellular dopamine and induced motor stereotypy. Both of these effects were potentiated by tolcapone. The rate of dopamine biosynthesis decreased when reuptake was inhibited. These data provide evidence for the key role of the dopamine transporter in maintaining neurochemical homeostasis at the synaptic level.

Animals↗
PubMed1998

Further evidence for interaction between angiotensin II and dopamine receptors (experiments on apomorphine stereotypy).

The present study was undertaken to further evaluate the effects of angiotensinergic agents: angiotensin II (AII), its analogues sarmesin ([Sar1, Tyr(Me)4]AII) and sarilesin ([Sar1, Ile8]AII), as well as DuP 753, a nonpeptide selective AT1 receptor antagonist, on apomorphine stereotypy in rats thus providing further evidence for AII-DAergic receptor interactions. All drugs were administered intracerebroventricularly (i.c.v.). Stereotyped behavior was evoked by an i.p. injection of 3 mg/kg apomorphine. AII (0.1-5 micrograms) exerted a decrease on stereotypies (U-shaped); the effect being significant at doses of 1 and 2 micrograms. Sarmesin significantly increased apomorphine stereotypy at a dose of 5 micrograms and decreased it at a dose of 20 micrograms. Sarmesin (10 micrograms) reversed the decreasing effect of AII (2 micrograms) leading to a more pronounced increase of stereotypies. Sarilesin (5 micrograms), which by itself is inactive, also demonstrated antagonistic properties when injected 5 min before AII (2 micrograms). DuP 753 (100 micrograms) alone had no significant effect on apomorphine stereotypy, but injected 5 min before AII (2 micrograms) it reversed the decreasing effect of AII on stereotypy. Taken together, the results further confirm the hypothesis that AII closely interacts with DAergic neurotransmission, an effect which is mediated predominantly by AT1 receptors.

Angiotensin II↗
PubMed1990

Pharmacologic and toxicologic effects of di(beta-phenylisopropyl)amine (DPIA) in rats and mice.

1. Di(beta-phenylisopropyl)amine (DPIA) given i.p. to mice and rats in sublethal doses caused increased motility, mild stereotypic behavior and suppression of food intake. Repeated daily doses led to enhanced motor stimulation, and in one group, 40% lethality, indicating development of "reverse tolerance". Brain monoamine modifiers prevented DPIA-induced motor activity. 2. Treatment with toxic i.p. doses of DPIA enabled determination of the LD50, which was 106.8 mg/kg for isolated mice and 89.7 mg/kg for mice kept in aggregation after dosing. Possible antidotal agents given before a high DPIA dose (LD50) protected significantly against lethality. 3. Combinations of DPIA with (+)-amphetamine in mice at lethal doses showed a subadditive synergism. 4. Effects of DPIA on the cardiovascular system, both i.v. in anesthetized rats and in isolated atrial preparations, were mainly opposite to those of (+)-amphetamine, namely decreases in blood pressure, force of contraction and heart rate.

Amphetamine↗
PubMed1994

Sensitization to stereotypy in DBA/2J but not C57BL/6J mice with repeated cocaine.

The present study investigated the effects of seven repeated daily injections of 32 mg/kg cocaine on stereotyped behaviors (repetitive locomotion, rearing, and head bobbing) in two genetically distinct strains of mice. An initial injection of cocaine induced no stereotypy in either DBA/2J or C57BL/6J mice. Following the fourth daily injection, cocaine induced stereotypies in DBA/2J mice (11.33 +/- 4.40) compared to saline controls (2.67 +/- 1.54). Cocaine-induced stereotypy in DBA/2J mice was further enhanced following the seventh daily injection (19.83 +/- 4.39) as compared to saline controls (0.67 +/- 0.54). No cocaine-induced stereotypy was observed in C57BL/6J mice following any injection. Eighth day saline challenges of cocaine-sensitized mice did not induce stereotypy. Eighth day cocaine challenges of saline-treated mice induced no stereotypy in either strain. The current study demonstrates that sensitization to cocaine can be influenced by genotype and suggests that genetically defined animals may be useful in elucidating mechanisms underlying sensitization and tolerance to cocaine.

Animals↗
PubMed1990

Dopaminergic alterations in cotreatments attenuating haloperidol-induced hypersensitivity.

Chronic treatment of the laboratory rat with haloperidol results in an increased stereotypic behavioral response to subsequent dopamine agonist challenge. This behavioral hypersensitivity (BH) is thought to reflect an increase in DA receptor number following chronic pharmacologic denervation. Using a cotreatment strategy, we demonstrate here that a variety of agents can attenuate or prevent the development of BH when administered chronically with haloperidol. Cotreatment with lithium and amantadine prevented the changes in DA biochemistry as well as the proliferation of DA receptors normally associated with chronic haloperidol treatment. Cotreatment with thioridazine or scopolamine did alter the changes in DA biochemistry normally associated with haloperidol treatment, but failed to attenuate the DA receptor proliferation. Taken together, these data suggest that mechanisms in addition to DA biochemical and receptor changes participate in the development and subsequent expression of BH. DA receptor proliferation must, therefore, be considered permissive to the development of BH.

Amantadine↗
PubMed1995

Apomorphine produced more yawning in Sprague-Dawley rats than in F344 rats: a pharmacological study.

Apomorphine induced yawning in both Sprague-Dawley and F344 rats in the same dose range, but F344 rats emitted only about 1/4 as many yawns as did Sprague-Dawley rats. At higher doses, rats of both strains exhibited stereotypic behavior with a comparable intensity. Pretreatment with either SCH 23390 [R(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-o l] or pindolol increased apomorphine-induced yawning further in Sprague-Dawley rats, but had little effect on the low yawning score produced by apomorphine in F344 rats. The low yawning response to apomorphine in F344 rats is, therefore, not due to a high baseline dopaminergic or adrenergic activity. Apomorphine-induced yawning in F344 rats was increased after an acute injection of physostigmine, or 24 h after an injection of reserpine. It is postulated that a low baseline cholinergic activity in F344 rats may be responsible, in part, for their lower yawning response to dopaminergic receptor stimulation.

Adrenergic alpha-Antagonists↗
PubMed1995

Role of the cerebellar fastigial nucleus in the physiological regulation of cerebral blood flow.

Local cerebral blood flow (ICBF) was measured with [14C]iodoantipyrine in conscious, unrestrained rats during electrical stimulation of the fastigial nucleus (FN). Electrode position in the FN was determined by blood pressure (MABP) responses to stimulation under anesthesia. In nine rats in which MABP responses had been variable under anesthesia, bipolar stimulation (50 Hz, 0.5 ms, 1 s on/1 s off) with currents of 30-100 microA after recovery from anesthesia produced stereotypic behavior but little effect on MABP and ICBF. In seven other conscious rats currents could be raised to 75-200 microA without inducing seizures, resulting in sustained MABP elevations during the ICBF measurement and significantly increased ICBF in the sensory-motor (+45%), parietal (+31%), and frontal cortices (+56%) and the caudate-putamen (+27%) above control values (n = 9). Glucose utilization, measured with [14C]deoxyglucose, in rats similarly stimulated was significantly increased in six structures, including some of the above, indicating increases in ICBF due to metabolic activation. Unilateral or bilateral electrolytic lesions of the FN, placed 6-7 days before ICBF measurement, had negligible effects on resting ICBF and on autoregulation in conscious rats. These results fail to support a specific role for the FN in physiological regulation of cerebral blood flow in unanesthetized rats.

Anesthesia↗
PubMed2007

Caudate nucleus is enlarged in high-functioning medication-naive subjects with autism.

BACKGROUND: Autism is defined by three symptom clusters, including repetitive and stereotyped behavior. Previous studies have implicated basal ganglia in these behaviors. Earlier studies investigating basal ganglia in autism have included subjects on neuroleptics known to affect basal ganglia volumes. Therefore, we investigated these structures in medication-naive subjects with autism. METHODS: Volumetric magnetic resonance measures of caudate, putamen, and nucleus accumbens were compared in two independent samples of medication-naive, high-functioning subjects with autism or Asperger syndrome: 1) 21 affected children and adolescents and 21 matched control subjects; and 2) 21 affected adolescents and young adults and 21 matched control subjects. RESULTS: Caudate nucleus was enlarged in both samples. This result remained significant after correction for total brain volume. CONCLUSIONS: These results implicate caudate nucleus in autism, as an enlargement of this structure was disproportional to an increase in total brain volume in two independent samples of medication-naive subjects with autism.

Adolescent↗
PubMed1992

AMPA glutamate receptor activation in the posterior zona incerta inhibits amphetamine- and apomorphine-induced stereotypy.

Previous work demonstrated that alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) glutamate receptor antagonism in the zona incerta (ZI) dorsal to the subthalamic nucleus inhibits stereotypy in rats. The current investigation was undertaken to determine if AMPA receptors in a more caudal portion of the ZI have a role in the expression of stereotyped behavior. Rats were injected bilaterally with AMPA into the posterior ZI dorsal to the substantia nigra, and immediately given a systemic injection of d-amphetamine (10 mg/kg, s.c.) or apomorphine (1 mg/kg s.c.). AMPA produced a dose-dependent inhibition of stereotypy induced by both drugs which was prevented by the coadministration of the AMPA/kainic acid antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX) (0.5 microgram/0.5 microliter). A dose of AMPA as low as 62.5 ng completely abolished the oral component of stereotypy induced by both apomorphine and amphetamine. This dose of AMPA alone had no significant effect on spontaneous locomotor activity but enhanced the locomotor response stimulated by amphetamine (10 mg/kg, s.c.) due to an inhibition of stereotypy. The finding that activation of AMPA receptors in the posterior ZI inhibits stereotypy shows a contrast to results in the neighboring medial ZI dorsal to the subthalamic nucleus, where blockade of AMPA/kainic acid glutamate receptors with DNQX inhibits stereotypy.

Animals↗
PubMed1998

Neurobehavioral effects of anandamide and cannabinoid receptor gene expression in mice.

The objective of the present study was to determine the neurobehavioral effects of the putative endogenous cannabinoid ligand, anandamide, and its influence on cannabinoid (CB1) receptor gene expression. The effect of acute administration of anandamide to C57BL/6, DBA/2, and ICR mice were evaluated in motor function and emotionality tests. The C57BL/6 and ICR mouse strains were more sensitive than the DBA/2 strain to the depression of locomotor activity and stereotyped behavior caused by anandamide. Although anandamide produced catalepsy in all three strains, anandamide induced ataxia in the minus-maze test only in the C57BL/6 animals and only at the lowest dose used. In the plus-maze test system, anandamide produced a mild aversive response, and by the third day of treatment the mouse strains developed an intense aversion to the open arms of the plus-maze. Northern analysis data using the recently cloned mouse cannabinoid receptor cDNA as a probe indicated that there was abundant expression of CB1 gene in the whole brain of the ICR mouse than in the brains of the C57BL/6 and DBA/2 strains with or without pretreatment with anandamide. The anandamide induced neurobehavioral profile does not seem to correspond to the CB1 gene expression in the mouse strains. It is, therefore, unlikely that the CB1 receptor mediates all the cannabinomimetic effects of anandamide in the brain.

Animals↗
PubMed1984

Systematic comparison of apomorphine-induced behavioral changes in two mouse strains with inherited differences in brain dopamine receptors.

Dosage and time dependencies of apomorphine-induced changes in stereotyped behaviors (climbing, gnawing and sniffing), locomotor activity and rearing activity were compared in young adult male mice of two inbred strains, DBA/2 and C57BL/6. These two strains are known to differ in their genetically specified brain dopamine receptor number. Apomorphine administered intraperitoneally at dosages of 0.5-20 mg/kg failed to induced stereotyped climbing in DBA/2 at any of the doses tested but markedly increased climbing in C57BL/6 at higher dosages. Apomorphine-induced stereotyped gnawing occurred in both strains at higher dosages although the latency was shorter and maximal effect greater in C57BL/6. Stereotyped sniffing was induced in both strains to a comparable degree at doses greater than or equal to 2.0 mg/kg, and the duration of this stereotypy was indistinguishable between strains. Locomotor activity was inhibited maximally in DBA/2 at an apomorphine dosage of 2 mg/kg and was inhibited to a greater extent than was C57BL/6. Rearing was inhibited in both strains by doses of apomorphine greater than or equal to 0.5 mg/kg; however the duration of the effect was considerably greater in DBA/2 than in C57BL/6. These data suggest that genetically determined differences in central dopamine receptors may have profound and selective effects on behaviors mediated by dopamine pathways; that complex behavioral patterns, e.g., apomorphine-induced stereotypy, may be dissected in to individual components by identifying neuropharmaco genetic differences between strains; that marked strain-specific, inherited differences in dopamine agonist-induced behavioral changes do occur among inbred, non-mutant mouse strains and that their occurrence in other mammalian species including man should be considered.

Animals↗
PubMed1986

Desenkephalin-gamma-endorphin restores the impaired sensitivity of hypophysectomized rats to small doses of apomorphine.

Hypophysectomized male rats, tested 7 days after removal of the pituitary, showed a reduced sensitivity to small doses of apomorphine. In these rats, subcutaneous (s.c.) treatment with apomorphine (25, 100 or 250 micrograms/kg) did not elicit any reduction in locomotor activity measured 5 min after injection in contrast to that observed in sham-operated control rats. The enhancement of locomotor activity and stereotyped behavior, 20 min after the s.c. administration of apomorphine, was similar in hypophysectomized rats and in control animals. Prolactin does not seem to be implicated in this altered sensitivity, since hyperprolactinaemia induced by pituitary homografts under the kidney capsule did not change the response to apomorphine in hypophysectomized rats. Chronic treatment with desenkephalin-gamma-endorphin (DE gamma E), a beta-endorphin fragment with neuroleptic-like properties, administered s.c. twice a day for 7 days at the dose of 10 micrograms/rat, restored the sensitivity to small doses of apomorphine in the hypophysectomized rats. The data suggest that removal of the pituitary leads to impaired sensitivity of presumably presynaptically located dopamine receptors mediating the effects of small doses of apomorphine without altering the sensitivity of postsynaptically located dopamine receptors that mediate the hypermotility and stereotypy induced by apomorphine. This impaired sensitivity to low doses of apomorphine could be restored by DE gamma E but not by prolactin, supporting the conclusions from previous experiments that DE gamma E and prolactin may selectively interfere with pre- and postsynaptic dopamine receptors respectively.

Animals↗
PubMed1991

The response to acoustic stimulation and the changes in brain amine levels after repeated administration of beta-phenylethylamine in rats.

Reverse tolerance to stereotyped behavior was induced after repeated administration of beta-phenylethylamine (PEA) (50 mg/kg, i.p., daily for 10 days) in rats. The reverse tolerance was maintained for at least 4 weeks after the last administration. We studied the effects of acoustic stimulation on locomotor activity 2 days and 4 weeks after withdrawal from PEA and measured the changes in brain monoamine levels 4 weeks after the withdrawal. Locomotor activity during acoustic stimulation was increased in the saline treated group, and this response was unaffected after repeated PEA treatment. Four weeks after withdrawal, significant increases in noradrenaline levels in the cerebral cortex and decreases in 5-hydroxytryptamine levels in the hypothalamus were found. The effects of acoustic stimulation on locomotor activity and the changes in brain monoamine levels were different from those of methamphetamine treatment obtained in our previous study. In conclusion, it may be suggested that the response to acoustic stimulation after repeated PEA administration in rats cannot be a model for abnormal responsiveness to environmental stimulation that is observed in chronic paranoid schizophrenics.

Acoustic Stimulation↗
PubMed1981

Modification of motor activity, passive avoidance conditioning and evoked potentials by microinjections of strychnine in both caudate nuclei in cats.

Passive avoidance conditioning (PAC) seems to depend on inhibitory actions within the caudate nucleus (CN). Thus topical application of strychnine could block these influences. In cats, with permanently implanted cannulae in the head of the CN, bilateral microinjections of 100 micrograms of strychnine produced a stereotyped behavior of grooming and running with the extremities flexed to dark places. When placed into a two compartment chamber for a PAC acquisition they would not move from the dark compartment to the illuminated one. After decreasing the illumination some cats crossed and the acquisition test was performed. Twenty four hours later they showed the learned response. A second retention test was not modified by another strychnine application. These results contrast with those obtained by picrotoxin microinjections which disrupt the retention of a PAC. However, strychnine affects the evoked potentials (EP) recorded in CN by n. centralis medialis (NCM) stimulation by decreasing a positive peak, which probably represents post-synaptic inhibition and increasing the late positive component. In the lateral geniculate body strychnine affected a late positive wave and in the occipital cortex it increased the initial negative peaks and decreased the late positive ones of the potentials evoked by flash stimulation. These findings suggest a more suitable role of the CN in the regulation of visual information, which is probably related with the attention processes.

Animals↗
PubMed1981

Synthesis and neuroleptic activity of benzamides. Cis-N-(1-benzyl-2-methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-(methylamino)benzamide and related compounds.

Three series of benzamides of N,N-disubstituted ethylenediamines (linear alkane-1,2-diamines), 1-substituted 2-(aminomethyl)pyrrolidines, and 1-substituted 3-aminopyrrolidines (cyclic alkane-1,2-diamines) were designed and synthesized as potential neuroleptics. All target compounds were evaluated for their inhibitory effects on apomorphine-induced stereotyped behavior in rats, and a good correlation between structure and activity was found throughout the series. In the linear series (analogues of metoclopramide), introduction of a benzyl group on the terminal nitrogen, rather than an ethyl group, and a methyl group on the p-amino group of metoclopramide both enhanced the activity. The resulting N-[2-(N-benzyl-N-methylamino)ethyl]-5-chloro-2-methoxy-4-(methylamino) benzamide(23) was about 15 times more active than metoclopramide. In the cyclic series, particularly among the benzamides of 1-benzyl-3-aminopyrrolidine, most of the compounds tested were more active than the corresponding linear benzamides. cis-N-(1-Benzyl-2-methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-(methylamino) benzamide (YM-09151-2, 55) was the most active among all of the compounds tested, being 13 and 408 times more potent than haloperidol and metoclopramide, respectively. Moreover, compound 55 exhibited a fairly high ratio of antistereotypic activity to cataleptogenicity compared with haloperidol and metoclopramide. It is expected that compound 55 may be used as a potent drug with few side effects in the treatment of psychosis.

Animals↗