Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CATALEPSY”

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

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

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of metergoline, fenfluramine, and 8-OHDPAT on catalepsy induced by haloperidol or morphine.

The influences of the indirect serotonin agonist fenfluramine (5; 10 mg/kg s.c.), the serotonin antagonist metergoline (5; 10 mg/kg s.c.) and the 5-HT1A agonist 8-OHDPAT (0.1; 0.2; 0.46 mg/kg s.c.) on haloperidol-induced catalepsy in rats or mice and on morphine-induced catalepsy in rats were studied. Morphine-induced catalepsy was enhanced by fenfluramine and attenuated by metergoline, whereas neither fenfluramine nor metergoline had any effect on haloperidol-induced catalepsy. 8-OHDPAT strongly antagonised catalepsy induced by morphine or haloperidol. We conclude that serotonergic transmission plays a major role in effectuating morphine catalepsy but not in effectuating haloperidol catalepsy. The antagonistic effect of 8-OHDPAT suggests a secondary, modulating role for 5-HT1A receptor mediated events in both types of catalepsy.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1985

Evidence for a cholinergic role in haloperidol-induced catalepsy.

Experiments in mice tested previous evidence that activation of cholinergic systems promotes catalepsy and that cholinergic mechanisms need to be intact for full expression of neuroleptic-induced catalepsy. Large doses of the cholinomimetic, pilocarpine, could induce catalepsy when peripheral cholinergic receptors were blocked. Low doses of pilocarpine caused a pronounced enhancement of the catalepsy that was induced by the dopaminergic blocker, haloperidol. A muscarinic receptor blocker, atropine, disrupted haloperidol-induced catalepsy. Intracranial injection of an acetylcholine-synthesis inhibitor, hemicholinium, prevented the catalepsy that is usually induced by haloperidol. These findings suggest the hypothesis that the catalepsy that is produced by neuroleptics such as haloperidol is actually mediated by intrinsic central cholinergic systems. Alternatively, activation of central cholinergic systems could promote catalepsy by suppression of dopaminergic systems.

Animals↗
PubMed1985

Experimental catalepsy is both enhanced and disrupted by apomorphine.

In mice that were scored for the length of time they remained immobile in awkward postures (cataleptic) on an inclined wire grid, a large IP dose of pilocarpine (80 mg/kg) caused a clear catalepsy, which was prevented by both dopamine agonists that were tested, apomorphine (4 or 8 mg/kg, IP) and bromocriptine (8 mg/kg, IP). In other experiments, haloperidol (2.5 mg/kg) caused mild catalepsy. As expected, neither 4 nor 8 mg/kg apomorphine caused much effect when given alone, but both doses produced profound and long-lasting catalepsy in the haloperidol-treated animals. Bromocriptine also had little effect when given alone, and neither 4 nor 8 mg/kg enhanced the haloperidol catalepsy. Apomorphine alone produced catalepsy at low doses. Repeated testing after a low (0.3 mg/kg) dose of apomorphine showed that catalepsy was most profound at 5 min postinjection, with progressive decline thereafter. Apomorphine, but not bromocriptine, thus can produce catalepsy under certain conditions of DA receptor blockade or in low dose. Catalepsy, and perhaps other forms of hypomotility, appear to be differentially mediated by a subclass of dopaminergic receptors.

Animals↗
PubMed1982

Unilateral injection of morphine into the nucleus accumbens induces akinesia and catalepsy, but no spontaneous muscular rigidity in rats.

The role of the nucleus accumbens in the generation of the signs of morphine-induced "catatonia" namely akinesia, catalepsy and muscular rigidity, was studied in rats. Morphine was injected into the nucleus accumbens and either spontaneous locomotor activity or catalepsy or activity in the electromyogram of the gastrocnemius-soleus muscle, signalling the appearance of rigidity, were recorded. Unilateral injections of 5 micrograms of morphine induced a decrease of locomotor activity and weak catalepsy; 15 micrograms of morphine completely abolished locomotor activity (akinesia) and produced a very pronounced catalepsy. All these effects were antagonized by naloxone (2 mg/kg i.p.). Injections of morphine into the nucleus accumbens did not induce muscular rigidity. In contrast, injection of morphine (15 micrograms) into the head of the caudate nucleus, which induced a pronounced muscular rigidity, did not noticeably alter the locomotor activity nor did it produce catalepsy. Our results suggest that 1) the nucleus accumbens is relevant for systemically administered morphine to produce akinesia and catalepsy, but is not noticeably involved in the development of muscular rigidity; 2) they provide evidence that morphine-induced catalepsy is largely due to a strong akinesia, and that muscular rigidity, observed after morphine administration, does not contribute to positive scores in the catalepsy test.

Animals↗
PubMed1987

Possible neuronal mechanisms involved in neurotensin-induced catalepsy in mice.

The neuronal mechanisms of neurotensin (NT)-induced catalepsy were investigated in mice. NT administered intracerebroventricularly (ICV 0.5, 1.0 and 2.0 micrograms) produced catalepsy in a dose-dependent fashion. A significant effect was observed at 2.0 micrograms and a maximal effect 2-3 h after injection. The NT-induced catalepsy was inhibited by pretreatment with atropine, trihexyphenidyl or biperiden (each drug, 0.8-5.0 mg/kg, IP), anticholinergic drugs, and L-DOPA (100, 200 mg/kg, IP). However, the catalepsy was not significantly antagonized by p-chlorphenylalanine (300 mg/kg X 3 days, IP) or methysergide (5, 10 mg/kg, IP), antiserotonergic drugs, and was not potentiated by the GABAergic drugs, aminooxyacetic acid (25 mg/kg, IP) or muscimol (1 mg/kg, IP). In addition, the NT-induced catalepsy was dose-dependently reduced by antihistamines, such as diphenhydramine (0.8-10 mg/kg, IP) and tripelennamine (0.4-5.0 mg/kg, IP) and was potentiated after treatment with histidine (250, 500 mg/kg, IP), a precursor of brain histamine. NT-induced catalepsy was also reduced by ICV pretreatment with diphenhydramine (1-5 micrograms/rat), a H1 antagonist, but not by cimetidine (5, 20 micrograms/rat), a H2 antagonist. These findings suggest that the catalepsy induced by NT may involve not only central cholinergic and dopaminergic mechanisms but also a histaminergic mechanism mediated via H1-histamine receptors, and seems to differ from the catalepsy induced by neuroleptics.

Animals↗
PubMed1995

Glucocorticoids attenuate haloperidol-induced catalepsy through adrenal catecholamines.

To examine the influence of adrenal secretions on neuroleptic induced catalepsy, we studied the effect of adrenocorticoids, noradrenaline (NA) or adrenaline (AD) on haloperidol (HAL) induced catalepsy in adrenalectomised (ADX) and sham-adrenalectomised (sham-ADX) rats. HAL (1 mg/kg, i.p.) induced a greater degree of catalepsy in ADX rats as compared to sham-ADX rats. Corticosterone (CORT, 1-2 mg/kg, s.c.) or dexamethasone (1-2 mg/kg, s.c.) attenuated the HAL catalepsy in sham-ADX but not in ADX rats. Further, when the HAL (1 mg/kg) catalepsy score was maximal (at 120 min), the rats were subjected to cold stress (3 degrees C for 10 min) or treated with NA, AD (2 micrograms/kg, i.v.) or CORT (2 mg/kg, s.c.). After cold stress procedure or CORT treatment, the catalepsy was significantly reduced in sham-ADX but not in ADX rats, whereas NA or AD infusion caused an immediate but short lasting significant decrease in HAL catalepsy in both sham-ADX and ADX rats. The anticataleptic effect of NA or glucocorticoids was blocked by an alpha 1 adrenoceptor blocker, prazosin. These findings suggest that peripheral noradrenergic and adrenergic mechanisms play an important role in the neuroleptic induced catalepsy. Such mechanisms may mediate the anticataleptic action of glucocorticoids.

Adrenalectomy↗
PubMed1993

Opposite effects of NMDA and AMPA receptor blockade on catalepsy induced by dopamine receptor antagonists.

Excitatory amino acid antagonists have been proposed as novel therapeutic agents for Parkinson's disease due to their ability to reverse akinesia in animal models of this disorder. To further evaluate this therapeutic potential, we examined the effects of a N-methyl-D-aspartate (NMDA) and an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist on catalepsy produced by dopamine D1 or D2 receptor antagonists in rats. Male Sprague-Dawley rats were injected with dizocilpine (MK-801 0.025, 0.05 or 0.1 mg/kg i.p.), 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX 12.5 mg/kg i.p.) or saline prior to administration of either raclopride (2.5 mg/kg i.p.) or SCH 23390 (0.5 mg/kg i.p.). Catalepsy was evaluated with both grid and bar tests every 20 min for 2.7 h. MK-801 (0.1 mg/kg) reversed the catalepsy produced by either raclopride or SCH 23390 but did not stimulate locomotion when given alone at this dose. At 0.05 mg/kg, MK-801 markedly decreased SCH 23390-induced catalepsy, but did not affect the catalepsy produced by raclopride. In contrast, NBQX increased raclopride-induced catalepsy, but had no effect on catalepsy elicited by SCH 23390. These findings suggest that blockade of NMDA receptors, but not non-NMDA receptors, may reverse the catalepsy produced by dopamine receptor antagonists.

Animals↗
PubMed1990

The effect of serotonergic agents on haloperidol-induced catalepsy.

The effect of various classes of serotonergic agents on haloperidol-induced catalepsy was evaluated in male Sprague-Dawley rats. The 5-HT-1A agonists buspirone, ipsapirone and 8-OH-DPAT all potently reversed catalepsy. The mixed 5-HT-1A and 5-HT-1B agonist RU 24969 reversed catalepsy only at the highest dose tested. The non-selective 5-HT-1 antagonist (l)-propranolol did not affect catalepsy. The 5-HT-2 agonist DOI and 5-HT-2 antagonist mesulergine both reversed catalepsy. ICS 205-930 (5-HT-3 antagonist) reversed catalepsy at low doses only. Another 5-HT-3 antagonist, GR 38032F, had no effect on catalepsy. These studies suggest that 5-HT-1A and 5-HT-2 receptor sites are important in the serotonergic modulation of haloperidol-induced catalepsy.

Animals↗
PubMed1995

Effects of 5-HT3 receptor antagonists on neuroleptic-induced catalepsy in mice.

Typical neuroleptics (e.g. haloperidol) can induce a cataleptic state in rodents by means of striatal DA receptor blockade. It has been shown that drugs which influence central serotonergic (5-HTergic) mechanisms can modify neuroleptic-induced catalepsy, suggesting that dopaminergic transmission is under 5-HTergic modulation. The aim of this study was to examine the effects of bemesetron and granisetron, two selective 5-HT3 receptor antagonists, on this catalepsy in mice. Catalepsy was induced with haloperidol (1.5 mg/kg, i.p.) and measured at 30-min intervals by means of a bar test. Drugs (or saline, for the controls) were injected i.p. 20 min before haloperidol, with each animal used only once. Bemesetron significantly reduced catalepsy at a dose of 1 mg/kg, whilst 10 mg/kg potentiated the phenomenon and 0.1 mg/kg was found to be without effect. Granisetron inhibited catalepsy at doses of 0.04 and 0.1 mg/kg while 4 mg/kg of the antagonist significantly increased the duration of catalepsy. These data suggest that 5-HT3 receptors play a role in neuroleptic-induced catalepsy. Considering the high affinities of both antagonists for 5-HT3 receptors, it is tempting to speculate that the potentiation of catalepsy by high doses of them is due to non 5-HT3 receptor mechanisms.

Animals↗
PubMed2005

Novel antipsychotic agents with 5-HT(1A) agonist properties: role of 5-HT(1A) receptor activation in attenuation of catalepsy induction in rats.

Compounds possessing 5-HT(1A) agonist properties attenuate catalepsy induced by D(2) receptor blockade. Here we examined the role of 5-HT(1A) receptor agonism in the reduced cataleptogenic potential of several novel antipsychotic agents in the crossed leg position (CLP) and the bar catalepsy tests in rats. When administered alone, ziprasidone produced marked catalepsy, whereas aripiprazole, bifeprunox, SLV313, SSR181507 and sarizotan did not. However, when 5-HT(1A) receptors were blocked with the selective antagonist, WAY100635 (0.63 mg/kg, SC), robust cataleptogenic properties of SLV313, bifeprunox and sarizotan were unmasked and the catalepsy induced by ziprasidone was accentuated. In contrast, only modest catalepsy was induced by aripiprazole and SSR181507, even following a higher dose of WAY100635 (2.5 mg/kg). This suggests that these compounds possess other anti-cataleptic properties, such as partial agonism at dopamine D(2) receptors. The capacity to reverse neuroleptic-induced catalepsy was investigated in interaction studies with haloperidol (2.5 mg/kg, SC). Whereas ziprasidone and aripiprazole did not markedly reduce the effects of haloperidol, SLV313 and sarizotan attenuated CLP catalepsy. In contrast, SSR181507 and bifeprunox potently inhibited both CLP and bar catalepsy. Taken together, these data show that 5-HT(1A) receptor activation reduces the cataleptogenic potential of novel antipsychotic agents but indicate marked diversity in the contribution of 5-HT(1A) and/or other mechanisms to the profiles of the drugs.

Analysis of Variance↗
PubMed2000

Haloperidol catalepsy consolidation in the rat as a model of neuromodulatory integration.

Haloperidol, a non-selective D(2) dopamine antagonist, both in vitro (1 microM) and in vivo (2.5 mg/kg i.p.), induced a long-term potentiation of K(+)-induced Ca(2+)-dependent release of endogenous noradrenaline and dopamine in rat brain cortical slices, by increasing the content of noradrenaline and dopamine known to be controlled by dopamine auto- and heteroreceptors. Haloperidol administration (2.5 mg/kg i.p.) evoked catalepsy and increased the content of noradrenaline and dopamine in the same structures of the brain. Haloperidol catalepsy consolidated without any additional learning and could be retrieved up to two weeks later by placing the animals in the test box. The catalepsy is disordered and retrieved only in the test box. The catalepsy was more intense on day 14 than on day 7. Injection of haloperidol immediately after conditioning evened the reflex retrieval on the following days. Moreover, learning increased the intensity of catalepsy in animals tested on the day of injection. Repeated testing of the reflex on the following days led to specific modifications of catalepsy retrieval. Pre-conditioned rats exhibited maximal catalepsy when tested immediately after being placed in the test box. These results suggest that both the processes of long-term potentiation and catalepsy consolidation are mediated by the same type of receptors, long-term modulation-inducing receptors. Endogenous neuromodulators, acting non-specifically or diffusely via their respective long-term modulation-inducing receptors, can initiate and consolidate generalized states which form the basis for emotional and motivational states.

Animals↗
PubMed2003

Catalepsy intensifies context-dependently irrespective of whether it is induced by intermittent or chronic dopamine deficiency.

It is well known that neuroleptic-induced catalepsy in rats intensifies upon repeated testing. Here, the question is addressed whether intensification of catalepsy results from intermittent drug administration or from intermittent context exposure. In experiment 1, rats were treated with intermittent haloperidol injections (0.25 mg/kg) followed by the catalepsy test (descent latency from the horizontal bar). In experiment 2, rats were lesioned with 6-hydroxydopamine injections into the striatum, resulting in a 45% reduction of dopamine concentration. Catalepsy was tested intermittently for several weeks. In both experiments we found a very stable intensification of catalepsy over 9 (haloperidol rats) and 11 (lesioned rats) days, showing that intensification is not due to intermittent dopamine depletion. In both experiments, intensification of catalepsy was very stable and was observed 18 days later in haloperidol-treated rats and 101 days later in lesioned animals. However, a change of the environmental context abolished the intensified catalepsy in both experiments. It is concluded that intensification of catalepsy is due to intermittent context exposure rather than intermittent drug administration. It is generally accepted that 6-hydroxydopamine lesions represent an animal model of Parkinson's disease. Given the results above, context-dependent intensification of parkinsonian symptoms might also occur in Parkinson's disease, and its prevention should be taken into consideration for future therapy of the disease.

Animals↗
PubMed1999

Role of adenosine and N-methyl-D-aspartate receptors in mediating haloperidol-induced gene expression and catalepsy.

Acute blockade of dopamine D(2) receptors by the typical antipsychotic drug haloperidol leads to alterations in neuronal gene expression and behavior. In the dorsolateral striatum, the levels of mRNA for the immediate-early gene c-fos and the neuropeptide gene neurotensin/neuromedin N (NT/N) are significantly increased by haloperidol. An acute behavioral response to haloperidol is catalepsy, considered to be a rodent correlate of some of the immediate extrapyramidal motor side effects seen in humans. Several lines of evidence suggest a link between neurotensin induction in the dorsolateral striatum and catalepsy. We hypothesize that both striatal gene induction and catalepsy elicited by haloperidol arise from the combined effect of excitatory adenosinergic and glutamatergic inputs acting at adenosine A(2A) and N-methyl-D-aspartate (NMDA) receptors, respectively. In agreement with our previous reports, adenosine antagonists reduced haloperidol-induced c-fos and neurotensin gene expression as well as catalepsy. In agreement with other reports, the noncompetitive NMDA receptor antagonist MK-801 also reduced gene expression and catalepsy in response to haloperidol. The competitive NMDA receptor antagonist LY235959 decreased haloperidol-induced catalepsy. We show here that blocking both A(2A) and NMDA receptors simultaneously in conjunction with haloperidol resulted in a combined effect on gene expression and behavior that was greater than that for block of either receptor alone. Both c-fos and NT/N mRNA levels were reduced, and catalepsy was completely abolished. These results indicate that the haloperidol-induced increases in c-fos and NT gene expression in the dorsolateral striatum and catalepsy are driven largely by adenosine and glutamatergic inputs acting at A(2A) and NMDA receptors.

Animals↗
PubMedDate not supplied

Central action of narcotic analgesics. I. Catalepsy and stereotypy in rats and narcotic analgesics.

The action of four analgesics, belonging to various pharmacological groups (morphine, codeine, fentanyl, pentazocine), was investigated in rats in tests for catalepsy and stereotypy, the tests depending on dopaminergic brain mechanisms. Interactions of the analgesics with a number of compounds known to affect dopaminergic brain functions in tests of catalepsy and stereotypy were also studied. In some experiments nalorphine, an antagonist of narcotic analgesics, was used. Morphine, codeine and fentanyl produced catalepsy, while pentazocine, at doses up to 60 microgram/kg, did not produce this effect. Reserpine, 2 mg/kg 3 hr before drugs, potentiated catalepsy produced by analgesics, while haloperidol, 0.2 mg/kg, 2 hr earlier, did not influence morphine and codeine catalepsy, but moderately potentiated fentanyl-induced catalepsy. alpha-methyl-p-tyrosine potentiated the cataleptogenic action of fentanyl and codeine, and also, less markedly, the action morphine. D-amphetamine (2.5-10 mg/kg) and apomorphine (5 mg/kg) moderately antagonized the catalepsy induced by analgesics, while atropine did not affect it. Nalorphine, 5 mg/kg, effectively abolished the catalepsy produced by narcotic analgesics, but did not affect that produced by neuroleptics. Morphine, codeine and fentanyl slightly inhibited apomorphine stereotypy, and evidently antagonized stereotypy produced by amphetamine. Pentazocine did not affect or slightly potentiated the both types of stereotypy. It is concluded that morphine, codeine and fentanyl, in contrast to pentazocine, inhibit behavioral activities depending on central dopaminergic functions in the rat. The mechanism of this action is most probably indirect, and seems to be related to the dopaminergic presynaptic functions.

Animals↗
PubMed1983

Cholinergic-dopaminergic interactions in experimental catalepsy.

The 'pinch-induced' model of catalepsy in the mouse was disrupted by atropine sulfate (4 mg/kg IP), confirming an earlier finding, and also by the antinicotinic mecamylamine (4 mg/kg). Either anticholinergic, when given concurrently with haloperidol (5 mg/kg), interfered with the typical haloperidol-induced enhancement of catalepsy. In mice pretreated with a peripheral cholinergic blocker, the cholinomimetic pilocarpine (10 mg/kg) enhanced catalepsy. The dopamine (DA) agonist apomorphine (5 mg/kg) reversed the enhancement that was normally caused by pilocarpine. Apomorphine did not stimulate open field locomotion in mice that were pretreated with pilocarpine. This lack of correlation between catalepsy and open field activity indicates that catalepsy in a unique state that involves more than mere absence of movement. The DA mechanisms, thus, appear to be specifically antagonistic to catalepsy or, conversely, cholinergic mediation of catalepsy involves reduced influence of DA systems.

Animals↗
PubMed1990

Synergistic effects between D-1 and D-2 dopamine antagonists on catalepsy in rats.

The effect of selective D-1 and D-2 dopamine agonists on catalepsy induced by various dopamine antagonists was studied. A potent and selective D-2 antagonist, YM-09151 (YM-09151-2) at a dose of 1.2 mg/kg, SC and a selective D-1 antagonist, SCH 23390 at 1.0 mg/kg, SC induced catalepsy in rats. Mixed D-1/D-2 antagonists, haloperidol (HPD) and cis-flupentixol (FLU) also induced catalepsy at doses of 2.0 and 0.8 mg/kg, SC, respectively. A mixed D-1/D-2 agonist, apomorphine (1.0 mg/kg, SC), a selective D-2 agonist, bromocriptine (10 mg/kg, IP) and a muscarinic antagonist, scopolamine (1.0 mg/kg, SC), prevented or markedly reduced the incidence of catalepsy by the tested antagonists. In contrast, a selective D-1 agonist, SKF 38393 (4.0 mg/kg, SC) did not reduce the cataleptogenic effects of HPD, FLU and SCH 23390, but did reduce the effect of YM-09151. Moreover, co-administration of YM-09151 with SCH 23390 produced a marked increase in the incidence of catalepsy. The incidence seen after the combination of YM-09151 and SCH 23390 at low doses was significantly different from that seen after each drug alone at the doubled dose. Thus, D-1 and D-2 antagonists potentiated each other's effect in producing catalepsy. These results suggest an important role of both D-1 and D-2 receptors in the catalepsy and the existence of synergistic effects of D-1 and D-2 receptor blockade.

Animals↗
PubMed1994

Distinct sites of dopaminergic and glutamatergic regulation of haloperidol-induced catalepsy within the rat caudate-putamen.

Previous studies have indicated that corticostriatal glutamatergic pathways are implicated in the regulation of neuroleptic catalepsy. To obtain a better understanding of the way in which dopamine (DA) and glutamate interact within the caudate-putamen (CP) in the development of catalepsy, we investigated the regional distribution within the rat CP of the cataleptogenic effect of haloperidol and its antagonism by D(-)-2-amino-5-phosphonopentanoic acid (D(-)AP5), a selective antagonist of the N-methyl-D-aspartate (NMDA) glutamate receptor subtype. Bilateral injections of haloperidol (3 micrograms/side) into the rostral ventromedial (VM) CP induced potent catalepsy with a short latency after the injection. In contrast, only a weak cataleptic response, of slower onset, was observed after haloperidol injections into the rostral ventrolateral (VL), rostral dorsomedial (DM), or rostral dorsolateral (DL) CP, or into the nucleus accumbens. D(-)AP5 (5 micrograms/side) injected bilaterally into the dorsorostral CP (DM and DL) strongly inhibited the catalepsy induced by systemic haloperidol (1 mg/kg, i.p.), and this effect lasted longer when the drug was injected into the DM than when it was injected into the DL. D(-)AP5 did not affect haloperidol-induced catalepsy when injected into the ventrorostral (VM and VL) or intermediate dorsal CP. D(-)AP5 injected into the DM, the region most sensitive to the anticataleptic effect of the drug, had no effect on basal levels of DA and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, or on the modification of these levels by haloperidol in either the DM or VM. These findings suggest that, while the catalepsy resulting from DA receptor blockade by haloperidol originates mainly from the VM, the expression of this phenomenon depends on an intact glutamatergic transmission within the dorsorostral CP. In the development of neuroleptic catalepsy, the mesencephalostriatal DAergic and corticostriatal glutamatergic pathways seem to be functionally linked through an indirect, rather than a direct, interaction.

2-Amino-5-phosphonovalerate↗
PubMed1985

Catalepsy induced by SCH 23390 in rats.

The ability of SCH 23390 as compared to haloperidol to produce catalepsy in rats was evaluated in three tests for catalepsy. SCH 23390 produced catalepsy in all three tests with ED50 (mg/kg s.c.) of 0.017 on the vertical grid, 0.023 on the horizontal bar and 0.038 on the 'four corks'. Haloperidol produced catalepsy with ED50 (mg/kg s.c.) of 0.048 on the vertical grid, 0.042 on the horizontal bar and 0.065 on the four corks. Catalepsy by SCH 23390 and by haloperidol was prevented by scopolamine and potentiated by alpha-methyl-p-tyrosine pretreatment. Catalepsy induced by SCH 23390 was also prevented by specific D-2 receptor agonists such as pergolide, lisuride and bromocriptine but not by the D-1 receptor agonist SKF 38393. The results demonstrate that SCH 23390 is potently cataleptogenic and that the catalepsy it produces has a pharmacologic profile typical of that produced by potent and specific D-2 antagonists.

Animals↗