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PubMed1982

Neurotensin induces catalepsy in mice.

Intracerebroventricular (i.c.v.) injection of neurotensin (NT) induced catalepsy in mice at doses greater than or equal to 0.02 microgram. The cataleptic effect progressively increased, reaching a maximum at approx. 2 hr after injection. In contrast, the hypothermic effect of neurotensin reached a maximum 1 hr after the injection, and was declining at 2 hr. Not all mice that showed hypothermia also showed catalepsy, and some mice showed catalepsy without hypothermia. Catalepsy induced by intracerebroventricular injection of neurotensin was not significantly correlated with the hypothermia. Furthermore, oxotremorine induced hypothermia without catalepsy. Thus, several lines of evidence indicate that the catalepsy induced by neurotensin is not the consequence of the neurotensin induced hypothermia. Thyrotropin releasing hormone (TRH), injected either intracerebroventricularly with neurotensin, or intraperitoneally before neurotensin abolished the hypothermia but only diminished the catalepsy scores. The cataleptic effect of neurotensin is consistent with its other neuroleptic-like activities.

Animals↗
PubMed1981

Involvement of caudate nucleus, amygdala or reticular formation in neuroleptic and narcotic catalepsy.

Local injection of haloperidol into the caudate nucleus produced catalepsy in contrast to the weak effects of morphine injected at the same site. Injection of either haloperidol or morphine into the amygdala did not have any cataleptogenic effect. Both haloperidol and morphine produced catalepsy when injected into the reticular formation. Naloxone injected into the reticular formation completely reversed the catalepsy following intraperitoneal morphine but not haloperidol. Pretreatment with alpha-methyl-p-tyrosine potentiated the effect of haloperidol injected into either the reticular formation or caudate nucleus. Phentolamine but not lignocaine or metergoline, injected into the reticular formation also caused a cataleptic response. The results confirm the caudate nucleus as a site for haloperidol catalepsy and in addition, suggest the reticular formation as a primary site for morphine catalepsy and a secondary site for haloperidol catalepsy; additionally a noradrenergic modulation of catalepsy may occur within this brainstem region.

Amygdala↗
PubMed1985

Neuroleptic-induced catalepsy: a D2 blockade phenomenon?

Typical neuroleptics, such as haloperidol, are cataleptogenic. But since such drugs block both D1 and D2 receptors, it is not clear if there is a differential receptor role in catalepsy. To test this issue in a mouse model of catalepsy, these experiments tested molindone, a D2-blocking neuroleptic with almost no ability to block D1 receptors. If D1 receptor blockade is necessary for catalepsy, molindone should not cause catalepsy. But molindone was cataleptogenic, albeit less potent than haloperidol. There was also a "training effect" with haloperidol, but not saline or molindone, in that the catalepsy produced by 5 mg/kg of haloperidol was much greater when tests were performed repeatedly at short intervals after injection. Concurrent administration of apomorphine (4 or 8 mg/kg) markedly potentiated haloperidol catalepsy, but had no effect on molindone catalepsy. Such results are not readily interpretable solely in terms of current concepts of D1 and D2 receptors.

Animals↗
PubMed1991

Catalepsy produced by striatal microinjections of the D1 dopamine receptor antagonist SCH 23390 in neonatal rats.

Systemic injection of the D1 dopamine receptor antagonist SCH 23390 produces catalepsy that is of lesser magnitude in neonatal than in adult rats. The present experiments were conducted in order to determine if SCH 23390 would produce catalepsy in neonatal rats following intrastriatal injection and if the ontogenetic pattern of catalepsy induced by intrastriatal SCH 23390 would be similar to the pattern observed with systemic injections. Rat pups (11 or 28 days of age) were microinjected unilaterally with SCH 23390 (0.2, 1, 5 or 10 micrograms) and tested for catalepsy using the forepaw-on-horizontal-bar test. The results demonstrated that robust catalepsy occurred at both ages following intrastriatal injection and that catalepsy induced by 5 micrograms SCH 23390 was of lesser magnitude in 11-day-olds than in 28-day-olds. A separate study assessed the distribution of [3H]SCH 23390 (5 micrograms) following intrastriatal injection in 28-day-olds. Results of the distribution study indicated that [3H]SCH 23390 was localized primarily within the striatum. Taken together, these results suggest that the striatal mechanisms for catalepsy produced by D1 receptor blockade are present, but not fully mature, in preweanling rat pups.

Age Factors↗
PubMed1991

Blockade of both D-1 and D-2 dopamine receptors may induce catalepsy in mice.

1. The catalepsy induced by dopamine antagonists has been tested and the possible dopamine subtypes involved in catalepsy was determined. 2. Dopamine antagonist fluphenazine, D-1 antagonist SCH 23390 or D-2 antagonist sulpiride induced catalepsy. The effect of fluphenazine and sulpiride was dose-dependent. Combination of SCH 23390 with sulpiride did not induce catalepsy potentiation. 3. D-1 agonist SKF 38393 or D-2 agonist quinpirole decreased the catalepsy induced by fluphenazine, SCH 23390 or sulpiride. 4. Combination of SKF 38393 with quinpirole did not cause potentiated inhibitory effect on catalepsy induced by dopamine antagonists. 5. The data may indicate that although D-2 receptor blockade is involved in catalepsy, the D-1 receptor may plan a role.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Dopamine increase in the prefrontal cortex correlates with reversal of haloperidol-induced catalepsy in rats.

The mechanism by which forced swimming reverses, haloperidol-induced catalepsy was examined by measuring dopamine (DA) turnover in the nucleus accumbens-ventromedial caudate (NAC-C) and the prefrontal cortex (PFC) in rats. DA and its metabolites 3,4-dihydroxiphenylacetic acid (DOPAC) and homovanillic acid (HVA) were assessed by microdialysis and high pressure liquid chromatography with electrochemical detection (HPLC-ED) after systemic administration of a cataleptic dose of haloperidol (5 mg/kg) or saline. Haloperidol-induced catalepsy was temporarily suppressed by forced swimming. Haloperidol-treated rats showed an increase of DA, DOPAC, and HVA overflow in the PFC and the NAC-C. This increase was greater in the PFC of rats that were forced to swim. Rats that were not treated with haloperidol but were forced to swim (control group) showed an increase of DA, DOPAC, and HVA in the PFC but not in the NAC-C. Zero micrograms, 5 micrograms, 10 micrograms, and 20 micrograms of DA was bilaterally injected in the PFC of cataleptic rats to evaluate the hypothesis that DA in the PFC reverses catalepsy. Haloperidol-induced catalepsy was diminished by bilateral microinjections of 10 micrograms and 20 micrograms but not by 5 micrograms of DA in the PFC. The higher the dose of DA, the longer the decrease of catalepsy. These results suggest that an increase of DA turnover in the PFC might mediate temporal suppression of haloperidol-induced catalepsy. The mechanism by which the mesocortical DA system reduces catalepsy is discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

Involvement of 5-hydroxytryptamine1A receptors in Delta9-tetrahydrocannabinol-induced catalepsy-like immobilization in mice.

The present study investigated the involvement of 5-hydroxytryptamine(1A) (5-HT(1A)) receptors in Delta(9)-tetrahydrocannabinol (THC)-induced catalepsy-like immobilization in mice. THC (10 mg/kg, i.p.) induced catalepsy-like immobilization but had no effect on motor coordination in the rota-rod test. The selective cannabinoid CB(1) receptor antagonist rimonabant (3 mg/kg, i.p.) completely antagonized THC-induced catalepsy-like immobilization. The 5-HT(1A)/5-HT(7) receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 0.3 and 1 mg/kg, i.p.) and 5-HT(1A) receptor partial agonist buspirone (0.06 and 0.1 mg/kg, i.p.) inhibited this THC-induced catalepsy-like immobilization. Moreover, the selective 5-HT(1A) receptor antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclohezane carboxamide dihydrochloride (WAY100635; 0.3 or 1 mg/kg, i.p.) reversed the inhibition of THC-induced catalepsy-like immobilization by 8-OH-DPAT (1 mg/kg) or buspirone (0.06 mg/kg). In contrast, the selective 5-HT(7) receptor antagonist (R)-3-[2-[2-(4-methylpiperidin-1-yl)ethyl]pyrrolidine-1-sulfonyl]phenol hydrochloride (SB269970) had no effect on this inhibitory effect of 8-OH-DPAT. On the other hand, WAY100635 (0.3 and 1 mg/kg, i.p.) enhanced the catalepsy-like immobilization induced by THC (6 mg/kg, i.p.). These findings suggest that the 5-HT(1A) receptors are involved in THC-induced catalepsy-like immobilization.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

5-HT1A receptor activation and anti-cataleptic effects: high-efficacy agonists maximally inhibit haloperidol-induced catalepsy.

Studies have shown that 5-HT1A receptor ligands modulate antipsychotic-induced catalepsy. Here, we further examined the role of intrinsic activity at 5-HT1A receptors in these effects. The anti-cataleptic effects of 5-HT(1A) receptor ligands with positive intrinsic activity [from high to low: 3-chloro-4-fluorophenyl-(4-fluoro-4-[[(5-methyl-6-methylamino-pyridin-2-ylmethyl)-amino]-methyl]-piperidin-1-yl-methanone fumaric acid salt (F 13714), eptapirone, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), 2-[4-[4-(7-methoxy-1-naphtyl) piperazino]butyl]-4-methyl-2H,4H-1,2,4-triazin-3,5-dione maleic acid salt (F 11461), buspirone, 2-[4-[4-(7-benzofuranyl)piperazino]butyl]-4-methyl-2H,4H-1,2,4-triazin-3,5-dione (F 12826), ipsapirone, and (s)-N-tert-butyl-3-(4-(2-methoxyphenyl)piperazine-1-yl)-2-phenylpropanamide hydrochloride (WAY 100135)] and negative intrinsic activity [N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohexanecarboxamide dihydrochloride (WAY 100635)] were examined. Catalepsy was induced by the classical antipsychotic haloperidol (0.63 mg/kg) and measured in the cross-legged position test and in the bar test. All 5-HT1A receptor agonists, except WAY 100135, significantly attenuated the effects of haloperidol in the cross-legged position test. All agonists had similar effects in the bar test, except ipsapirone, which failed to attenuate haloperidol-induced catalepsy. In contrast to the effects observed with the agonists, the inverse agonist WAY 100635 appeared to enhance haloperidol-induced catalepsy in both tests, in agreement with earlier findings. The maximal effects of the 5-HT1A receptor ligands to attenuate catalepsy correlated positively with the rank order of their intrinsic activity at 5-HT1A receptors (either catalepsy test: r(S)=0.92, P<0.001). F 13714, which had the highest intrinsic activity, maximally inhibited haloperidol-induced catalepsy in the cross-legged position and bar tests (100% and 99% inhibition, respectively). Because the magnitude of the anti-cataleptic effects of 5-HT1A receptor ligands correlates positively with their intrinsic activity, it is likely that F 13714 has marked anti-cataleptic effects because of its high intrinsic activity at 5-HT1A receptors.

Animals↗
PubMed2000

Haloperidol-induced catalepsy is absent in dopamine D(2), but maintained in dopamine D(3) receptor knock-out mice.

We have previously found that mice homozygous for the deletion of the dopamine D(2) receptor gene (D(2)(-/-) mice) do not present spontaneous catalepsy when tested in a "bar test". In the present study, we sought to analyse the reactivity of D(2) receptor mutant mice to the cataleptogenic effects of dopamine D(2)-like or D(1)-like receptor antagonists. In parallel, we assessed the cataleptogenic effects of these antagonists in dopamine D(3) receptor mutant mice. D(2)(-/-) mice were totally unresponsive to the cataleptogenic effects of the dopamine D(2)-like receptor antagonist haloperidol (0.125-2 mg/kg i.p.), while D(2)(+/-) mice, at the highest haloperidol doses tested, showed a level of catalepsy about half that of wild-type controls. The degree of haloperidol-induced catalepsy was thus proportional to the level of striatal dopamine D(2) receptor expression (0.50, 0.30 and 0.08 pmol/mg protein as measured at 0.25 nM [3H]spiperone for D(2)(+/+), D(2)(+/-) and D(2)(-/-) mice, respectively). However, D(2)(-/-) and D(2)(+/-) mice were as sensitive as their wild-type counterparts to the cataleptogenic effects of the dopamine D(1)-like receptor antagonist R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine hydrochloride (SCH 23390: 0.03-0.6 mg/kg s.c.). Striatal dopamine D(1) receptor expression (as measured using [3H]SCH 23390 binding) was not significantly affected by the genotype. The ability of SCH 23390 to induce catalepsy in D(2)(-/-) mice suggests that their resistance to haloperidol-induced catalepsy is due to the absence of dopamine D(2) receptors, and not to the abnormal striatal synaptic plasticity that has been shown by others to occur in these mice. In agreement with the observation that dopamine D(2) and dopamine D(1) receptor expression was essentially identical in D(3)(+/+), D(3)(+/-) and D(3)(-/-) mice, dopamine D(3) receptor homozygous and heterozygous mutant mice, on the whole, did not differ from their controls in the time spent in a cataleptic position following administration of either haloperidol (0.5-2 mg/kg i.p.) or SCH 23390 (0.03-0.6 mg/kg s.c.). Also, dopamine D(3) receptor mutant mice were no more responsive than wild-type controls when co-administered subthreshold doses of haloperidol (0.125 mg/kg) and SCH 23390 (0.03 mg/kg), suggesting that dopamine D(3) receptor knock-out mice are not more sensitive than wild-types to the synergistic effects of concurrent blockade of dopamine D(2) and dopamine D(1) receptors in this model. These results suggest that the dopamine D(2) receptor subtype is necessary for haloperidol to produce catalepsy, and that the dopamine D(3) receptor subtype appears to exert no observable control over the catalepsy produced by dopamine D(2)-like, D(1)-like and the combination of D(1)-like and D(2)-like receptor antagonists.

Animals↗
PubMed2003

Caffeine and muscarinic antagonists act in synergy to inhibit haloperidol-induced catalepsy.

The possible synergism between caffeine and muscarinic antagonists to inhibit haloperidol-induced catalepsy was investigated with the bar test in rats. Pretreatment with low doses of caffeine (1-3 mg/kg), a non-selective adenosine antagonist, dose dependently reduced the intensity and increased the onset latency of catalepsy induced by haloperidol (0.5-2 mg/kg). Similar effects were produced by the muscarinic antagonists atropine (4.1 mg/kg), and trihexyphenidyl (THP, 0.01-3 mg/kg). THP inhibited catalepsy intensity with an ED(50) of 0.38 mg/kg, and increased its onset latency with an ED(50) of 0.52 mg/kg. The anticataleptic effect of anticholinergics was potentiated when a low dose of caffeine (1 mg/kg) was applied simultaneously. In the presence of caffeine, THP inhibited catalepsy intensity with an ED(50) of 0.19 mg/kg, and prolonged the latency with an ED(50) of 0.30 mg/kg. The synergism was more evident when THP was administered at subthreshold doses that were unable to modify haloperidol-induced catalepsy when applied alone, but produced a clear inhibition of catalepsy when injected with caffeine. To assess whether repeated administration of caffeine could induce tolerance to the synergism with THP, a group of rats was pretreated with three daily doses of caffeine (1 mg/kg) for seven days, and the catalepsy test was performed on the eighth day. In these animals, caffeine was still able to enhance the anticataleptic actions of THP, suggesting that repeated administration of 1 mg/kg caffeine does not induce tolerance to the synergism with anticholinergics. These results indicate that low doses of caffeine enhance the anticataleptic actions of muscarinic antagonists, and leave open the possibility of using caffeine as adjunctive therapy to reduce the doses and the adverse effects of anticholinergics in Parkinson's disease.

Animals↗
PubMed1999

Evidence of sex related differences in the effects of calcium channel blockers on neuroleptic-induced catalepsy in mice.

1. Calcium channel blockers (CCBs) are reported to affect extrapyramidal motor behavior in mammals. Since sex related differences are a common feature in the pharmacological properties of several centrally active drugs, the authors decided to investigate the effects of verapamil (VER), flunarizine (FLU) and nimodipine (NIM), three pharmacologically different CCBs, on neuroleptic-induced catalepsy in male and female albino mice. 2. Catalepsy was induced with haloperidol (0.75 mg/kg, i.p.) and measured at 30-min intervals by means of a bar test. Drugs (or appropriate vehicle, for the controls) were injected i.p. 20 min before haloperidol, with each animal being used only once. 3. VER (1, 5 and 10 mg/kg) did not significantly affect catalepsy in male mice. In females, however, a significant attenuation of catalepsy was found at the two higher doses. 4. FLU (1, 5 and 10 mg/kg) did not significantly affect catalepsy in male mice, whilst a significant attenuation was observed in females with the doses of 1 and 5 mg/kg (but not with the dose of 10 mg/kg). 5. NIM (3, 10 and 30 mg/kg) potentiated neuroleptic-catalepsy in males at the doses of 10 and 30 mg/kg. In females, however, only the higher dose of NIM caused a potentiation of catalepsy. 6. These results demonstrate the existence of sex related differences in the extrapyramidal effects of CCBs in mice. Further, this sex related effect might depend, among other factors, on the particular channel involved.

Animals↗
PubMed1993

Catalepsy induced by muscimol infused into the hypothalamus can be sensitized and is modulated by ovarian steroids.

Muscimol (25 ng), but not saline, infused into the region of the zona incerta and lateral hypothalamus induced significant catalepsy in female rats. Daily administration of muscimol for 5 days resulted in a sensitization of the cataleptic response such that there was a significantly greater response to the same dose of muscimol beginning on Day 3 and continuing to increase up to Day 5. It was determined that the increase in catalepsy across days was not the result of conditioning after an initial exposure to muscimol. The endocrine condition of the female affected the degree of catalepsy induced by the first exposure to intrahypothalamic muscimol. Ovariectomized rats pretreated with estradiol benzoate (EB) exhibited significantly greater catalepsy than did females untreated or treated with progesterone or combined EB and progesterone. Weekly administration of muscimol also produced significant sensitization of the behavioral response, and the degree of sensitization was again affected by endocrine condition. Specifically, although females treated with EB for 2 days before muscimol infusion showed a significantly greater catalepsy after the first infusion than did ovariectomized females, they failed to show any increase in catalepsy scores across the 4 weeks of treatment. The greater catalepsy induced by muscimol infusion in EB-treated females may be related to changes in dopaminergic transmission. In contrast, females pretreated with progesterone 4 hr before muscimol infusion (with or without prior EB) exhibited highly significant increases in cataleptic response across the 4 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Haloperidol, but not clozapine, produces dramatic catalepsy in delta9-THC-treated rats: possible clinical implications.

The effect on rat catalepsy induced by Delta9-tetrahydrocannabinol (Delta9-THC) in association with haloperidol (HP) or clozapine (CLOZ) administration was investigated. Delta9-THC dose-dependently increased HP (0.05-1 mg kg-1, s.c.)-induced rat catalepsy, while no catalepsy was observed after CLOZ (1-20 mg kg-1, s.c.) or Delta9-THC+CLOZ administration. The CB1 antagonist SR141716A (0.5-5 mg kg-1, i.p.) reversed the increase mediated by Delta9-THC on HP-induced catalepsy. The D2 agonist quinpirole completely reversed the catalepsy induced by both HP and HP+Delta9-THC; however, higher doses of quinpirole were needed in the presence of Delta9-THC. The M1 antagonist scopolamine and alpha2 antagonist yohimbine were able to reduce the catalepsy induced by HP and HP+Delta9-THC in a similar manner. CLOZ and the 5-HT2A/2C antagonists ritanserin, RS102221 and SB242084 were more effective in antagonizing HP than HP+Delta9-THC-induced catalepsy.7 HP and CLOZ failed to inhibit in vitro [3H]CP-55,940 binding, while Delta9-THC and SR141716A did not show an appreciable affinity for the D2 receptor. It was suggested that the different effects on rat catalepsy induced by Delta9-THC following HP or CLOZ administration may depend on the receptor-binding profiles of the two antipsychotics. The preferential use of CLOZ rather than HP in the treatment of psychotic symptoms in cannabis abusers was discussed.

Animals↗
PubMed2000

Epilepsy and catalepsy in Anglo-American literature between romanticism and realism: Tennyson, Poe, Eliot and Collins.

Epilepsy and catalepsy were not clearly separated in the minds of people in the early 19th century, and catalepsy may have been used as a diagnostic euphemism for epilepsy. Tennyson, in "The Princess" describes, under the diagnosis of catalepsy, probable temporal lobe epileptic dreamy states with derealization which serve as a metaphor of sexual and moral ambivalence, the poem's central theme. It seems that Tennyson knew such seizures from his own father who had been given a diagnosis of catalepsy. Poe gave his Berenice in the novella of the same title a diagnosis of epilepsy as a reason for a premature burial. However, there was a good deal of unlikelyhood in this, and when he came to this theme in "The Fall of the House of Usher" and in "The Premature Burial" he chose instead a diagnosis of catalepsy which fitted better with the plot. The fits of the title character in George Eliot's Silas Marner, diagnosed as catalepsy, would today rather be seen as epileptic twilight states. It would seem that this author drew from contemporary dictionary descriptions which described conditions similar to Marner's fits under the heading of catalepsy. In Eliot's "legend with a realistic treatment", the twilight states are a central factor in the plot and explain Marner's reclusion and passivity. In Poor Miss Finch by English realist Wilkie Collins, the post-traumatic seizures of Oscar, one of the main characters, their cause, their treatment with silver nitrate, and the subsequent discoloration of his skin are central supporting elements of a perfectly constructed plot. Collins gives an exact description of a right versive seizure with secondary generalisation, and how to deal with it. In none of these works seizures are seen in a negative light. They rather evoke reactions of sympathy and support.

Catalepsy↗
PubMed2006

Selective breeding for catalepsy changes the distribution of microsatellite D13Mit76 alleles linked to the 5-HT serotonin receptor gene in mice.

Catalepsy (pronounced motor inhibition) is a natural defensive reaction against predator. Recently, the quantitative trait locus for catalepsy was mapped on mouse chromosome 13 near the 5-HT(1A) serotonin receptor gene. Here, the linkage between catalepsy and the 5-HT(1A) receptor gene was verified using breeding experiment. Selective breeding for high predisposition to catalepsy was started from backcross BC[CBA x (CBA x AKR)] generation between catalepsy-prone (CBA) and catalepsy-resistant (AKR) mouse strains. CBA and AKR strains also differed in the 5-HT(1A) receptor functional activity. A rapid increase of cataleptic percentage from 21.2% in the backcrosses to 71% in the third generation of selective breeding (S3) was shown. The fragment of chromosome 13 including the 5-HT(1A) receptor gene was marked with D13Mit76 microsatellite. Breeding for catalepsy increased the concentration of CBA-derived and decreased the concentration of AKR-derived alleles of microsatellite D13Mit76 in the S1 and S2. All mice of the S9 and S12 were homozygous for CBA-derived allele of D13Mit76 marker. Mice of the S12 showed CBA-like receptor activity. These findings indicate that selective breeding for behavior can involve selection of polymorphic variants of the 5-HT(1A) receptor gene.

Animals↗
PubMed2003

Quercetin potentiates L-Dopa reversal of drug-induced catalepsy in rats: possible COMT/MAO inhibition.

L-Dopa plus carbidopa treatment remains the first-line therapy in Parkinson's disease. The use of catechol-O-methyltransferase (COMT) and/or monoamine oxidase (MAO) inhibitors as an adjunct to L-dopa therapy has yielded varying degrees of success. Quercetin, a flavonoid present in many plants, is reported to inhibit COMT and MAO activities, the key enzymes involved in the metabolism of dopamine. In the present study we have studied the effect of quercetin on the L-dopa plus carbidopa combination against perphenazine and reserpine-induced catalepsy in rats. Neuroleptic-induced catalepsy is a widely accepted animal model for testing the drugs used in parkinsonism. Catalepsy in rats was induced by administration of perphenazine (5 mg/kg i.p.) or reserpine (2.5 mg/kg i.p.) + alpha-methyl-P-tyrosine (200 mg/kg i.p.). Catalepsy in animals was assessed by using the bar test. The quercetin dose (25-100 mg/kg, p.o.) dependently reversed perphenazine- as well as reserpine-induced catalepsy. When quercetin was combined with a subthreshold dose of L-dopa plus carbidopa, the anticatatonic effect was potentiated. Pretreatment with a central COMT inhibitor, 3,5-dinitrocatechol (OR-486) (10 mg/kg p.o.), or a MAO-B inhibitor, selegiline (5 mg/kg i.p.), also potentiated the actions of threshold dose of quercetin against perphenazine- or reserpine-induced catalepsy. On the other hand adenosine (100 mg/kg i.p.), which is known to decrease the release of catecholamines through an action on presynaptic A(1) receptors, partly reversed the protective effect of quercetin against perphenazine-induced catalepsy. Quercetin through its COMT and MAO enzyme-inhibiting properties might potentiate the anticatatonic effect of L-dopa plus carbidopa treatment. The results of the present study strongly suggest that quercetin could serve as an effective adjunct to L-dopa therapy in Parkinson's disease.

Animals↗
PubMed1983

Morphine may not produce true catalepsy.

Though catalepsy is one of the primary features classically associated with morphine injections in animals, several investigators have suggested that morphine may not produce true catalepsy. A study was therefore undertaken using the most widely accepted tests of catalepsy to determine whether a dose related catalepsy could be obtained in rats. The effect produced by morphine was then compared with the catalepsy elicited by subthreshold to suprathreshold doses of haloperidol. In the course of catalepsy assessment, it was found that half the tests employed could not distinguish between the several doses of morphine that were administered. Moreover, the cataleptoid behavior induced by morphine failed to satisfy nearly all of the criteria most widely used for catalepsy. This is in marked contrast to the results obtained with varying doses of haloperidol. These results are compatible with the suggestion that morphine may not be a true cataleptigenic agent.

Animals↗
PubMedDate not supplied

Effects of antidepressants and antihistaminics on catalepsy induced by intracerebroventricular administration of histamine in mice.

The intracerebroventricular (icv) administration of histamine but not N-telemethylhistamine and 1-methyl-4-imidazole acetic acid induced catalepsy in mice. Histamine H1-receptor blockers such as cyproheptadine, mepyramine and diphenhydramine reduced histamine-induced catalepsy. However, astemizole which is known to be without central effects, did not reduce histamine-induced catalepsy. The icv pretreatment with histamine H2-receptor blockers, such as metiamide and cimetidine, also had no effect. Moreover, various antidepressants, both imipramine- and atypical-type drugs antagonized histamine-induced catalepsy to various degrees in this experiment. Thus, the induction of catalepsy by icv administration of histamine was mediated through histamine H1-receptors, and suggested that antidepressants reduced histamine-induced catalepsy via this mechanism. Histamine-induced catalepsy is a possible new animal model of depression which can also be used for evaluation of atypical antidepressants.

Animals↗