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PubMed1999

[Genetic relationships between catalepsy and pendulum movements in rats].

Predispositions to pendulum movements (PMs) and catalepsy was studied in rat strains selected for predisposition to catalepsy and for enhanced or suppressed PMs. Positive correlation between PMs and catalepsy at earlier stages of selection changed to negative at later stages. Based on these data, it was hypothesized that the genes that determine the predisposition to catalepsy affect the expression of the gene determining PMs in such a way that different PM alleles become dominant in the cases of moderate and strong effects of the catalepsy genes.

Animals↗
PubMed1992

Effects of age and isolation on the evolution of catalepsy during chronic haloperidol treatment.

Sixteen young (5 months) and 16 old (20-24 months) male Wistar rats, housed together or in individual cages were observed for cataleptic behavior 10, 20 and 30 days after the beginning of chronic haloperidol treatment (1.0 mg/kg, twice daily, for 30 days). Catalepsy was measured by the bar test. Age increased the duration of haloperidol-induced catalepsy of isolated and group-housed rats in the three observation sessions (old-isolated = 7.4 +/- 0.2; old-group housed = 7.5 +/- 0.1; young-isolated = 6.3 +/- 0.2; young-group housed = 6.8 +/- 0.2 In seconds in session 1, for example). Conversely, isolation did not modify the sensitivity to the cataleptic effect of haloperidol. Even more important, no differences in duration of haloperidol-induced catalepsy were observed among the three sessions for each group. The results indicate that under the experimental conditions employed the animals did not develop tolerance nor sensitization to haloperidol-induced catalepsy. In addition, neither age nor isolation modified the absence of effects of repeated haloperidol treatment on the catalepsy behavior of rats.

Aging↗
PubMed2004

[Effect of experimental elevation and decrease of thyroxine level on catalepsy in rats].

Thyroid dysfunction is associated with mental disorders. The present study was aimed to reveal the effects of experimental decrease and increase of thyroxine level on expression of two types of extensive freezing: spontaneous and pinch-induced catalepsy, in Wistar rat males. Chronic administration of thyroxine synthesis inhibitor, propylthiouracil (5 mg/kg/day, 28 days), markedly decreased plasma hormone level and at the same time produced a significant increase in percentage of spontaneously cataleptic animals and immobility time, but had no effect on the expression of pinch-induced catalepsy. On the contrary, chronic thyroxin (0.1 mg/kg/day, 28 days) treatment produced no effect on spontaneous catalepsy expression, although it significantly increased percentage of cataleptic animals and immobility time of pinch-induced catalepsy. The results suggest that both the thyroid hormone deficit and excess provoke catalepsy in rats but enhance different forms of freezing reaction.

Animals↗
PubMedDate not supplied

[Does the catalepsy phenomenon reflect the functional dopaminergic activity in pharmacological investigations?].

The dynamics of spontaneous and haloperidol-induced catalepsy in mice has been studied. It is established that the degree of manifestation of the spontaneous catalepsy is directly related to the number of manipulations (mice standings in the "lector position"). At the same time, the intensity of catalepsy (both spontaneous and haloperidol-induced) was not related to the mice response to apomorphine injections. It is concluded that spontaneous catalepsy rather insignificantly influences the results of pharmacological tests, but this factor has to be taken into account in the study of physiological mechanisms. The absence of correlations between catalepsy manifestations and the apomorphine test results is indicative of complexity of the mechanism of this disorder and cannot be attributed entirely to the violation of dopaminergic processes in CNS.

Animals↗
PubMed1989

[The relation of tryptophan hydroxylase activity in the brain and the manifestation of catalepsy in mice].

Pinch-induced catalepsy and thyptophan hydroxylase (TPH) activity in striatum and midbrain were determined in male mice of 6 inbred strains. Pronounced catalepsy was found in the only mice strain--CBA. TPH activity in midbrain and especially in striatum of CBA mice was higher than in the strains, which did not display catalepsy. The experimental situation, which promotes the development of highly aggressive CBA males, caused a decrease in TPH activity in striatum and these mice did not express genetic predisposition to catalepsy. The results indicate that TPH activity in striatum is involved in the mechanism of catalepsy in mice.

Animals↗
PubMedDate not supplied

Influence of dopamine agonists and an opiate antagonist on agaricus-induced catalepsy, as tested by a new method.

A few drugs affecting the dopaminergic system were tested for cataleptic effects in mice, and compared with an orally administered plant extract, Agaricus Muscarius 30. Haloperidol, Agaricus, and a low dose of apomorphine (0.3 mg/kg) were cataleptic. Paralleling previously reported results with haloperidol, the Agaricus catalepsy was potentiated by the mixed agonist, apomorphine (5 mg/kg), and by the selective D2 agonist, bromocriptine (5 mg/kg) and was reversed by the D1 agonist, SKF 38393. Naloxone also reversed Agaricus catalepsy, suggesting an involvement of opiate as well as dopaminergic mechanisms. All conditions that produced catalepsy also suppressed spontaneous locomotion, except for Agaricus 30 given alone. These experiments also compared cataleptic drugs by the published "pinch" method that involves repeated trials with a new single-trial method. Catalepsy was produced by the same drugs in both tests, but the single-trial method was more sensitive for disclosing the catalepsy induced by weaker cataleptogens.

Agaricales↗
PubMed1993

Influence of median raphe nucleus lesions on neuroleptic-induced catalepsy and on the anticataleptic effect of buspirone.

Catalepsy induced by neuroleptics in rats can be modified by 5-hydroxytryptaminergic (5-HTergic) manipulation. For example, buspirone (BUS) and other central 5-HT1A receptor ligands reduce neuroleptic-induced catalepsy (NIC). The dorsal (DRN) and median (MRN) raphe nuclei are reported to be important sources of 5-HTergic projections to the basal ganglia, the site of action of neuroleptics in producing NIC. A previous study showed that lesion of DRN did not affect NIC or the anticataleptic effect of BUS. The present study was designed to evaluate the participation of MRN in NIC and in the anti-NIC effect of BUS. Twenty-four male Wistar rats (N = 6/group) weighing 220-250 g were used. Electrolytic lesion of MRN was carried out in anesthetized rats along with sham operations (electrode inserted but no current applied). Ten days later, the rats were injected with BUS (5 mg/kg, ip) or saline (1 ml, ip). Catalepsy was induced 20 min later with haloperidol (H; 1 mg/kg, ip) and measured at 30-min intervals by means of a bar test. The Costall & Naylor method of scoring (range 0-5 points) was used. Saline-injected MRN-lesioned rats displayed significantly lower catalepsy scores than sham-lesioned rats (1.5 +/- 0.2 vs 3.8 +/- 0.3 at 90 min after H). In sham-lesioned rats, BUS significantly reduced the catalepsy scores in comparison with saline-treated animals (1.3 +/- 0.2 vs 3.8 +/- 0.3 at 90 min after H). However, BUS was not able to further reduce NIC in the MRN-lesioned animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Nitric oxide donors antagonize N-nitro-L-arginine and haloperidol catalepsy: potential implication for the treatment of Parkinsonism?

Nitric oxide (NO) synthase inhibitor, N-nitro-L-arginine (NNLA) produced dose-dependent, long-lasting catalepsy in rats, the effect being attenuated by NO donors L-arginine and molsidomine. Catalepsy induced by haloperidol (0.4 mg/kg i.p.), D2 receptor antagonist, was reduced dose-dependently by molsidomine (10.0-100.0 mg/kg) and by L-arginine at a dose of 100.0 mg/kg. Low, non-cataleptic doses of NNLA (0.1 mg/kg) and haloperidol (0.1 mg/kg) given in combination produced a marked and long-lasting catalepsy. The results suggest that NO plays a role in NNLA-induced catalepsy as well as in catalepsy elicited by haloperidol.

Animals↗
PubMed1976

Influence of WA-335, a factor which blocks serotonin receptors, on neuroleptic-induced catalepsy.

In a previous study, anticataleptic action of cyproheptadine was reported. The present investigation deals with the influence of WA-335 (9,10-dihydro-10-(1-methyl-4-piperidylidene)-9-anthrol), another antagonist of serotonin, on catalepsy induced in rats with spiroperidol, pimozide, fluphenazine and reserpine. WA-335 antagonized catalepsy induced by these neuroleptics (the effect on reserpine-induced catalepsy was weakest). Joint administration of WA-335 and L-DOPA with an inhibitor of peripheral decarboxylase, or WA-335 and amantadine produced a stronger antagonistic effect (spiroperidol catalepsy) than either of these substances separately. WA-335 did not prevent catalepsy induced with physostigmine.

Amantadine↗
PubMed1997

Haloperidol-induced catalepsy: a model for screening antidepressants effective in treatment of depression with Parkinson's disease.

Incidence of severe depression is very common in Parkinson's disease (PD). Use of antidepressants in such cases is known to improve or worsen the existing PD. However, prediction of the effect of antidepressant on symptoms of PD is limited due to lack of suitable animal model. The present study examines the possibility of using haloperidol-induced catalepsy model in rats for this purpose. Antidepressants showed distinct effect on haloperidol-induced catalepsy, although most of them reduced forced-swimming induced immobility. In general, antidepressants with greater noradrenergic reuptake inhibition (desipramine, imipramine, amitriptyline, nortriptyline, protriptyline and maprotiline) reduced, whereas those with serotonergic reuptake inhibition (fluoxetine and clomipramine) increased haloperidol-induced catalepsy. Mianserin, an atypical antidepressant, and alprazolam, a benzodiazepine receptor analogue had no effect on haloperidol-induced catalepsy. The results suggest that haloperidol-induced catalepsy model in rats needs to be incorporated in the screening procedure when evaluating the utility of antidepressant drugs for the treatment of depression associated with PD.

Animals↗
PubMed1990

Simple disturbance of the dam in the neonatal period can alter haloperidol-induced catalepsy in the adult offspring.

Three experiments were performed to determine whether apparently minimal disturbances of dams and litters would influence haloperidol-induced akinesia. In Experiment I, Long-Evans hooded rats (a) were left unmanipulated, (b) received nestcage relocation and observation, (c) received nestcage relocation/observation and maternal separation, or (d) received nestcage relocation/observation and pup handling. The male adult offspring received open-field testing and later received forepaw-on-dowel catalepsy testing following saline, morphine (20 mg/kg), or haloperidol (2 mg/kg). In Experiment II, hooded rats received (a) no manipulation, (b) nestcage relocation, (c) maternal separation, or (d) pup handling. At weaning, dams were tested in the open-field. Activity wheel locomotion of the offspring was assessed following saline or haloperidol for 3 days/week for 3 weeks; then, 5 and 7 days later, rats received haloperidol (0.5 mg/kg) and catalepsy testing. In both experiments, manipulations involving the dam reduced the offsprings' haloperidol-induced catalepsy, but, in Experiment II, a history of haloperidol administration distinguished between the effects of nestcage relocation and maternal separation. In Experiment III, Swiss albino mice received (a) no treatment, (b) nestcage relocation and maternal separation, (c) relocation/separation and mild cold stress of pups, (d) relocation/separation and pup handling, or (e) relocation/separation and severe cold stress of pups. Adult male mice received saline or haloperidol (2.5 mg/kg) and inclined grid catalepsy testing. Mice receiving relocation/separation and mice receiving relocation/separation and severe cold stress showed enhanced catalepsy versus control mice. Thus, it was concluded that seemingly innocuous events in infancy can influence the intensity of extrapyramidal side effects of neuroleptics in adulthood.

Animals↗
PubMed1994

Lesions of the entopeduncular nucleus and the subthalamic nucleus reduce dopamine receptor antagonist-induced catalepsy in the rat.

The role of the entopeduncular nucleus (EP) and the subthalamic nucleus (STN) in mediating dopamine receptor antagonist-induced catalepsy in the rat was investigated. Five days after bilateral lesions of EP and STN respectively with the excitotoxin quinolinic acid (15, 30 nmol/0.5 microliter/side and 24 nmol/0.5 microliter/side, respectively) rats were injected intraperitoneally with the dopamine D1 receptor antagonist SCH 23390 (0.5 mg/kg) or the dopamine D2 receptor antagonist haloperidol (0.5 mg/kg). Complete EP lesions prevented both SCH 23390- and haloperidol-induced catalepsy. STN lesions exerted pronounced anticataleptic effects in case of haloperidol-induced catalepsy, but less pronounced in case of SCH 233390-induced catalepsy. Further characterization of these anticataleptic effects in an open field demonstrated, that neither EP- nor STN lesions reversed bradykinesia, which occurred after selective dopamine receptor blockade. In conclusion, both EP and STN participate in the mediation of catalepsy induced by dopamine D1- and dopamine D2 receptor antagonists. Thereby these nuclei preferentially mediate rigidity and akinesia, but to a lesser extent bradykinesia.

Animals↗
PubMed2001

NMDA receptor antagonists do not block the development of sensitization of catalepsy, but make its expression state-dependent.

Dopamine (DA) receptor blockade induces catalepsy in rats which increases in strength upon retesting. This increase in catalepsy represents a form of sensitization which has been shown to be completely context dependent. Sensitization of catalepsy therefore represents a good model for studying the neurobiological mechanisms underlying the interaction between the cellular effect of a drug (DA-receptor blockade) and the context. This study investigated whether glutamatergic mechanisms are involved in the development of sensitization. Rats were treated with either haloperidol or haloperidol plus an N-methyl-D-aspartate (NMDA) receptor antagonist. Haloperidol consistently induced catalepsy which developed sensitization upon retesting. Co-administration of D-CPPene (5 mg/kg and 10 mg/kg, i.p.), eliprodil (30 mg/kg, i.p.) or Ro 25-6981 (15 mg/kg, i.p.) did not have any effect on sensitization, although all three drugs exerted some anticataleptic effects. When sensitization developed under haloperidol plus NMDA receptor antagonist, the sensitized response was expressed only in the presence of the NMDA receptor antagonist. This strongly suggests that the NMDA receptor antagonists represent contextual stimuli to which catalepsy has been conditioned, and this implies that the expression of sensitization has been rendered state-dependent.

Animals↗
PubMed1998

Catalepsy induced by calcium channel blockers in mice.

It is known that calcium channel blockers induce Parkinsonism. In this study, amlodipine-, diltiazem-, and verapamil-induced catalepsy was investigated in mice. All of these three calcium channel blockers induced catalepsy. Dopamine D1, D2, and mACh receptor occupancies were estimated under the same conditions, and the affinities of these drugs for each receptor were also estimated in vitro. Intensity of catalepsy was predicted by dopamine D1, D2, and mACh receptor occupancies with the dynamic model which had already been constructed and was compared with the observed values. The predicted and the observed values were comparable (r = 0.98, p < 0.001). In conclusion, the dynamic model considering D1, and D2, and mACh receptor occupancy may be useful for quantitative prediction of drug-induced catalepsy.

Amlodipine↗
PubMed1993

Reversal of reserpine-induced catalepsy by selective D1 and D2 dopamine agonists.

To gain insight into the antiparkinsonian effects of selective D1 and D2 dopamine receptor stimulation, we examined the ability of D1 (SKF 38393) and D2 (quinpirole) agonists to reverse catalepsy induced by the combined administration of reserpine and alpha-methyl-p-tyrosine (AMPT) in rats. Catalepsy, the failure to correct an externally imposed posture, is a measure of akinesia and was assessed using the bar test. Rats injected with reserpine alone (2.5 mg/kg i.p.) developed akinesia and ptosis within 60-90 min. The D1 agonist SKF 38393 (30 mg/kg i.v.) rapidly reversed ptosis and restored near-normal mobility when administered 24 h after reserpine and AMPT; catalepsy was reversed for 90 min, after which the drug effect wore off. Quinpirole (1 mg/kg i.v.) reversed catalepsy for the duration of the test period (4 h) but did not consistently reverse ptosis or promote normal mobility; the rats continued to exhibit kyphotic postures with little spontaneous locomotion. These results indicate that selective D1 stimulation is sufficient to reverse reserpine-induced akinesia and highlight the need for the development of potent selective D1 agonists for clinical trial in Parkinson's disease. In severe dopamine depletion, D2 stimulation alone appears to be insufficient to restore normal movement. Quinpirole, but not SKF 38393, elicited paroxysmal limb/body jerking in reserpine-AMPT-treated rats, providing further evidence that atypical jerking can be elicited by D2 stimulation in the complete absence of D1 stimulation. This laboratory observation suggests that some jerking dyskinesias seen in treated parkinsonian patients may be mediated by an imbalance in D1-D2 receptor stimulation.

Animals↗
PubMed2005

3,4-Methylenedioxymethamphetamine counteracts akinesia enantioselectively in rat rotational behavior and catalepsy.

We have shown recently that 3,4-methylenedioxymethamphetamine (MDMA) has symptomatic antiparkinsonian activity in rodent models of Parkinson's disease. In search of its mechanism of action, we further investigated the enantiomers of MDMA in the rotational behavioral model and catalepsy test. Catalepsy testing was done in drug-naive unlesioned animals. The parkinsonian symptoms rigor and akinesia (i.e., catalepsy) were induced by intraperitoneal administration of haloperidol 0.5 mg/kg and measured repeatedly as descent latency from a horizontal bar and a vertical grid. MDMA and both its enantiomers were effective in counteracting haloperidol-induced catalepsy, but if given as racemic, the effects were more pronounced than with the enantiomers. For testing of rotational behavior, male Sprague Dawley rats were lesioned unilaterally with 6-hydroxydopamine (6-OHDA) at the medial forebrain bundle. Administration of S-MDMA (5 mg/kg) produced ipsilateral rotations. R-MDMA was far less effective in inducing ipsilateral rotations in 6-OHDA unilaterally lesioned rats, but when S-MDMA was given additionally rotations immediately increased. Regarding their overall antiparkinsonian effects, the S-enantiomer of MDMA was more effective than its R-congener. R-MDMA was able to increase the actions of S-MDMA.

Adrenergic Uptake Inhibitors↗
PubMed1977

Effect of muscarinic cholinergic drugs on morphine-induced catalepsy, antinociception and changes in brain dopamine metabolism.

The effects of drugs acting on muscarinic cholinergic receptors on the catalepsy, antinociception and changes in rectal temperature and in brain dopamine metabolism induced by morphine were studied in Wistar rats. Scopolamine (0.3 - 30 mg/kg) was about three times as potent as atropine (1 - 30 mg/kg) in potentiating the cataleptic effect of morphine. Methylscopolamine and methylatropine did not alter the cataleptic effect of morphine. Pilocarpine (100 mg/kg) and arecoline (10 mg/kg) slightly but significantly and RS86 (20 - 40 mg/kg) clearly antagonized the morphine-catalepsy. RS86 antagonized the atropine-induced potentiation of morphine catalepsy. The antinociceptive effect of pilocarpine was additive and that of RS86 less than additive with morphine. The antimuscarinic compounds did not alter the antinociceptive effect of morphine. Antimuscarinic compounds enhanced the hypothermic effect of morphine, but none of the compounds studied altered the hyperthermic effect of morphine. The antimuscarinic drugs reduced the concentration of striatal homovanillic acid (HVA) in about same proportion in control and morphine-treated rats. Both the muscarinic compounds and morphine increased the concentration of striatal HVA, but when combined their effects were not significantly different from those of morphine alone. Scopolamine antagonized and pilocarpine accelerated the morphine-induced increase in the rate of depletion of cerebral dopamine content. The present results show that the effects of muscarinic aand antimuscarinic cholinergic drugs on the cataleptic effect of morphine were opposite to their effects on the catalepsy induced by neuroleptic compounds.

Analgesia↗
PubMed1989

Difference in catalepsy response in inbred rats during chronic haloperidol treatment is not predictive of the intensity of behavioral hypersensitivity which subsequently develops.

An animal model was utilized to explore the observed clinical association between a history of significant neuroleptic-induced parkinsonism and an increased incidence for the subsequent development of tardive dyskinesia. Catalepsy-sensitive Fisher rats and catalepsy-resistant Brown Norway rats were treated for 14 days with haloperidol at a dose of either 1 mg/kg or 5 mg/kg daily. Following a 7-day drug withdrawal period, rats were tested for behavioral hypersensitivity to acute challenge with apomorphine and then striata were assayed for 3H-spiroperidol receptor binding. Despite significant interstrain difference in catalepsy response to either neuroleptic dose, Brown Norway rats treated with 5 mg/kg developed behavioral hypersensitivity and D-2 receptor supersensitivity equivalent to that of the similarly treated Fisher rats. Catalepsy, a possible rat analog for neuroleptic-induced parkinsonism, therefore did not predict the intensity of those subsequent behavioral and receptor changes considered to result from chronic antagonism of striatal dopamine receptors and to possibly underlie tardive dyskinesia. Further studies are required to elucidate the less than obvious relationship between extrapyramidal behavioral effects of chronic neuroleptic treatment.

Animals↗