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PubMed1995

Correlation between tryptophan hydroxylase activity in the brain and predisposition to pinch-induced catalepsy in mice.

Pinch-induced catalepsy and activity of the rate-limiting enzyme of serotonin biosynthesis, tryptophan hydroxylase, in brain structures have been studied in mice of six inbred strains. A pronounced predisposition to catalepsy was found in the CBA mouse strain. It was shown that the CBA mice had the highest tryptophan hydroxylase activity in the neostriatum compared to mice of other noncataleptic strains. The experience of repeated victories in intermale encounters producing highly aggressive CBA mice resulted in the inhibition of the genetically determined predisposition to pinch-induced catalepsy and in the simultaneous decrease of tryptophan hydroxylase activity in the neostriatum down to the level found in noncataleptic mice. The inhibitor of tryptophan hydroxylase, p-chloromethamphetamine, significantly decreased the enzyme activity in the neostriatum of CBA mice and completely inhibited their genetically determined predisposition to catalepsy. These findings indicate the key role of the striatal serotonergic system in the catalepsy-inducing mechanism.

Animals↗
PubMed1996

Effects of chronic methamphetamine on SCH23390- or haloperidol-induced catalepsy, and effects of coadministration of SCH23390 or haloperidol in mice.

The influence of chronic treatment of mice with methamphetamine, an indirect dopamine agonist, on the cataleptic effects of R-(+)-chloro-2,3,4,5,-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin -7ol hydrochloride (SCH23390), a D1 receptor agonist, or haloperidol, a mainly D2 antagonist, was investigated. Once every other day treatment with 3 mg/kg SC methamphetamine for 15 days resulted in an increase in the catalepsy produced by haloperidol (0.3 mg/kg IP) (haloperidol catalepsy), but in a decrease in the catalepsy produced by SCH23390 (0.3 mg/kg IP) (SCH23390 catalepsy), 24 h and 7 days after withdrawal of methamphetamine. These effects of chronic methamphetamine were antagonized by coadministration of either SCH23390 (0.5 mg/kg SC) or haloperidol (1.0 mg/kg SC). These results suggest that the decreased responsiveness to SCH23390 in chronic methamphetamine-pretreated mice results from a supersensitivity of D1 receptors, and that the increased responsiveness to haloperidol catalepsy results from a subsensitivity of D2 receptors. The attenuated response to SCH23390 may be interpreted as an example of sensitization to methamphetamine, and the enhanced haloperidol response as an example of tolerance to methamphetamine, based on the development of supersensitivity and subsensitivity of D1 and D2 receptors, respectively, after chronic methamphetamine administration. Furthermore, it is suggested that coadministration of either SCH23390 or haloperidol could prevent the development of D1 receptor supersensitivity and D2 receptor subsensitivity induced by chronic methamphetamine.

Animals↗
PubMed1989

Cholinergic maturation and SCH 23390-induced catalepsy in the male rat pup.

The cataleptogenic effects of the selective dopamine D1 receptor antagonist, SCH 23390, increased between 13 and 17 days of age in male pups. Seventeen- and 21-day-old pups showed equivalent catalepsy. Scopolamine blocked SCH 23390-induced catalepsy in 21-day-old pups but had little effect in 13-day-old pups. The development and cholinergic sensitivity of SCH 23390-induced catalepsy are similar to those seen after D2 or mixed D1/D2 receptor blockade. Cholinergic maturation appears to be an important component in the development of adult-like catalepsy, and the nature of a D1-acetylcholine interaction mediating catalepsy remains to be determined.

Aging↗
PubMed1988

D1- and D2-receptor antagonists induce catalepsy via different efferent striatal pathways [corrected].

The D1- and D2-receptor antagonists SCH 23390 and raclopride produced a dose-dependent catalepsy as studied by a vertical grid test in the male rat. The benzodiazepine antagonist Ro 15-1788 antagonized catalepsy induced by the D2-receptor antagonist raclopride while it failed to block the action of SCH 23390. The antimuscarinic drug scopolamine reduced and the gamma-aminobutyric acid (GABA) agonist muscimol enhanced catalepsy induced by both SCH 23390 and raclopride. The results suggest that D2-antagonist-induced catalepsy is mainly mediated via activation of the strio-pallidal GABA pathways whereas D1-receptor antagonist induced catalepsy is mainly mediated via increased activity in the nigrothalamic GABA pathways.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2004

Role of NMDA receptor subtypes in the induction of catalepsy and increase in Fos protein expression after administration of haloperidol.

The increase of Fos expression in the striatum induced by haloperidol, an antagonist of the dopamine D2 receptor, might be related to the activation of glutamatergic neurotransmission, especially that of N-methyl-D-aspartate (NMDA) receptors. In this study, using behavioral and immunohistochemical techniques, we examined the effects of a noncompetitive NMDA antagonist, (+)-MK-801, and an NMDA receptor NR2B subunit antagonist, ifenprodil, on catalepsy, an extrapyramidal symptom; in this context, we also considered the expression of Fos protein in the forebrain after the administration of haloperidol. Catalepsy in mice, induced by the administration of haloperidol (1 mg/kg), was inhibited by pretreatment with (+)-MK-801 (0.2 mg/kg) or ifenprodil (10 mg/kg). Furthermore, pretreatment with (+)-MK-801 (0.2 mg/kg) significantly attenuated the induction of Fos-immunoreactive (IR) cells in the dorsomedial, dorsolateral, and ventrolateral striatum, but not in the shell region of the nucleus accumbens after the administration of haloperidol, whereas pretreatment with ifenprodil (10 mg/kg) significantly attenuated the induction of Fos-IR cells in all of these areas. It is known that ifenprodil binds sigma receptors and alpha-1 adrenergic receptors with high affinity. Pretreatment with the sigma receptor antagonist BD-1407 (3 mg/kg) or the alpha-1 adrenergic receptor antagonist prazosin (3 mg/kg) affected neither catalepsy nor the expression of Fos-IR cells after the administration of haloperidol. However, pretreatment with CP-101,606 (1 mg/kg), a selective antagonist for the NR2B subunit of the NMDA receptor, significantly attenuated catalepsy and the expression of Fos-IR cells in the forebrain after the administration of haloperidol. These results suggest that the NMDA receptor antagonists attenuated the induction of catalepsy and Fos-IR cells in forebrain after the administration of haloperidol. It was also suggested that haloperidol-induced expression of Fos-IR cells in the shell region of the nucleus accumbens might be differentially regulated by NMDA receptor subunits. Therefore, it appears that selective antagonists for the NR2B subunit of the NMDA receptor (e.g., CP-101,606) might be useful drugs for the treatment of extrapyramidal side effects (EPS) associated with the chronic use of typical antipsychotics such as haloperidol.

Adrenergic alpha-Antagonists↗
PubMed1998

Tolerance to catalepsy following chronic haloperidol is not associated with changes in GABA release in the globus pallidus.

In vivo microdialysis was used to investigate the relationship between extracellular GABA levels in rat globus pallidus following acute (1st injection) and chronic (29th injection) haloperidol (Hal) (0.25 mg kg-1 day-1, s.c.) with the presence and absence of catalepsy, respectively. There was no difference in basal pallidal GABA levels in the drug naive and chronically treated rats. Furthermore, pallidal GABA release was not affected following injection with Hal in either group although there was a prolonged catalepsy in the drug naive group and a tolerance to catalepsy in the chronically treated group. A previous microdialysis study employing similar experiment protocol showed that Hal increases striatal GABA release in drug naive rats and increases basal striatal GABA levels following chronic treatment. The results of the current study demonstrate that these effects are not reflected in the globus pallidus and suggest that striatal GABA interneurons and/or GABA projection neurons to extrapallidal nuclei such as the substantia nigra pars reticulata may be involved in initiating catalepsy following acute Hal and mediating the tolerance to catalepsy observed following chronic Hal.

Animals↗
PubMed2002

Effect of the amisulpride isomers on rat catalepsy.

The substituted benzamide amisulpride is currently administered in its racemic form. In the present study, the biochemical and cataleptogenic profiles of the two enantiomers (R+ and S-) were compared with those of the racemic mixture. Displacement binding studies showed that the (S-)-isomer possesses an higher affinity for dopamine D2-like receptor (K(i) 5.2+/-0.4 nM) compared to (R+)-amisulpride (K(i) 244+/-12 nM) and to (RS)-amisulpride (K(i) 9.8+/-0.8 nM). In contrast, (S-)-amisulpride binds the alpha(2)-receptor with an affinity (K(i) 1528+/-45 nM) lower than that of the (R+)-isomer (K(i) 375+/-34 nM) and of (RS)-amisulpride (K(i) 783+/-27 nM). The bar test was used to evaluate the catalepsy induced by each drug. (RS)-amisulpride induced catalepsy only at very high doses (>100 mg/kg, s.c.) whereas, (S-)-amisulpride produced a catalepsy at a lower dose (30 mg/kg, s.c.) and (R+)-amisulpride did not produce any catalepsy up to the dose of 75 mg/kg. Interestingly, (R+)-amisulpride reduced the catalepsy induced by (S-)-amisulpride (50 mg/kg, s.c.) or haloperidol (0.3 mg/kg, s.c.), at the doses of 50 or 30 mg/kg, respectively. These results indicate that the weak cataleptic properties of (RS)-amisulpride might partially rely on its (R+)-isomer and provide a further explanation for the atypical properties of amisulpride as an antipsychotic.

Amisulpride↗
PubMed2003

Diminished catalepsy and dopamine metabolism distinguish aripiprazole from haloperidol or risperidone.

Catalepsy and changes in striatal and limbic dopamine metabolism were investigated in mice after oral administration of aripiprazole, haloperidol, and risperidone. Catalepsy duration decreased with chronic (21 day) aripiprazole compared with acute (single dose) treatment across a wide dose range, whereas catalepsy duration persisted with chronic haloperidol treatment. At the time of maximal catalepsy, acute aripiprazole did not alter neostriatal dopamine metabolite/dopamine ratios or homovanillic acid (HVA) levels, and produced small increases in dihydroxyphenylacetic acid (DOPAC). Effects were similar in the olfactory tubercle. Dopamine metabolism was essentially unchanged in both regions after chronic aripiprazole. Acute treatments with haloperidol or risperidone elevated DOPAC, HVA, and metabolite/dopamine ratios in both brain areas and these remained elevated with chronic treatment. The subtle effects of aripiprazole on striatal and limbic dopamine metabolism, and the decrease in catalepsy with chronic administration, illustrate fundamental differences in dopamine neurochemical actions and behavioral sequelae of aripiprazole compared to haloperidol or risperidone.

Administration, Oral↗
PubMed2002

Nicotine potentiation of morphine-induced catalepsy in mice.

In the present study, effects of nicotine on catalepsy induced by morphine in mice have been investigated. Morphine but not nicotine induced a dose-dependent catalepsy. The response of morphine was potentiated by nicotine. Intraperitoneal administration of atropine, naloxone, mecamylamine, and hexamethonium to mice reduced catalepsy induced by a combination of morphine with nicotine. Intracerebroventricular injection of atropine, hexamethonium, and naloxone also decreased catalepsy induced by morphine plus nicotine. Intraperitoneal administration of atropine, but not intraperitoneal or intracerebroventricular injection of hexamethonium, decreased the effect of a single dose of morphine. It was concluded that morphine catalepsy can be elicited by opioid and cholinergic receptors, and the potentiation of morphine induced by nicotine may also be mediated through cholinergic receptor mechanisms.

Animals↗
PubMed1984

The role of the GABA mechanisms of the globus pallidus in mediating catalepsy, stereotypy and locomotor activity.

Muscimol, picrotoxin and bicuculline were injected bilaterally through permanently implanted cannulae into either anterior (GPa) or posterior parts of the globus pallidus (GPp) of rats. Both the muscimol injected into the GPa and the picrotoxin injected into the GPp abolished or strongly inhibited spiperone (0.2 mg/kg, IP)-induced catalepsy. Muscimol alone (25-200 ng/0.2 microliter/GP) injected into the GPa evoked a dose-dependent biphasic effect: at first catalepsy (throughout 7.3 min), and then a long-lasting (more than 2 hr) locomotor stimulation and stereotyped sniffing. Muscimol (200 ng/GP) injected into GPp inhibited both the spontaneous motility and amphetamine-induced hyperactivity. Picrotoxin (200 and 400 ng/GP) injections into GPa and GPp produced an increase of the locomotor activity as well as stereotyped sniffing. Picrotoxin started to block muscimol hyperactivity when its own stimulatory action disappeared, thus also for picrotoxin the second phase of action could be detected. The globus pallidus is shown to be a relay station of impulses mediating neuroleptic catalepsy. Furthermore, it is suggested that behavioural changes induced by muscimol resulted from the action of the drug on at least 2 different neuronal systems, both being controlled by GABA receptors. One of them seems to be responsible for inducing neuroleptic-like catalepsy, and the other one for the hyperactivity and blockade of spiperone-catalepsy.

Animals↗
PubMed2002

Coadministration of L-NOARG and tiapride: effects on catalepsy in male mice.

This study was designed to determine the possible potentiation of catalepsy behavior after coadministration of N(G)-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase (NOS), and tiapride, a specific antagonist for D2 receptors, in male mice. Catalepsy was measured by the bar test. Two successive evaluations were carried out 60 and 90 min after injections. The induction of catalepsy following coadministration of L-NOARG (25 and 50 mg/kg) and tiapride (200 mg/kg) was significantly higher than the sum of catalepsy scores after administration of L-NOARG and tiapride separately. Coadministration of L-NOARG and tiapride produced a clear potentiation of their effects on catalepsy in mice. These results underline the view that nitric oxide (NO) interacts with central dopamine D2 transmission.

Animals↗
PubMed2003

The alpha 2-adrenoceptor antagonist idazoxan reverses catalepsy induced by haloperidol in rats independent of striatal dopamine release: role of serotonergic mechanisms.

The alpha(2)-adrenoceptor antagonist idazoxan may improve motor symptoms in Parkinson's disease and experimental Parkinsonism. We studied the effect of idazoxan on haloperidol-induced catalepsy in rats, an animal model of the drug-induced extrapyramidal side effects in man. Catalepsy was induced by a subcutaneous (s.c.) injection of haloperidol (1 mg/kg) and measured by the bar test for a maximum of 5 min. At 3 h after haloperidol, rats were given 0.16-5.0 mg/kg s.c. idazoxan, and descent latency was measured 1 h later. Idazoxan potently reversed haloperidol-induced catalepsy with an ED(50) of 0.25 mg/kg. This effect was mimicked by the selective alpha(2)-adrenoceptor antagonist RS-15385-197 (0.3 and 1 mg/kg orally). We assessed how dopaminergic mechanisms were involved in the anticataleptic effect of idazoxan by studying its effect on dopamine (DA) release in the striatum, with the microdialysis technique in conscious rats. Idazoxan (0.3 and 2.5 mg/kg) had no effect on extracellular DA and did not modify the rise of extracellular DA induced by haloperidol, indicating that changes of striatal DA release were not involved in the reversal of catalepsy. The anticataleptic effect of 2.5 mg/kg idazoxan (haloperidol+vehicle 288+/-8 s, haloperidol+idazoxan 47+/-22 s) was attenuated in rats given an intraventricular injection of 150 microg of the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (haloperidol+vehicle 275+/-25 s, haloperidol+idazoxan 137+/-28 s). The 5-HT(1A) receptor antagonist WAY100 635 (0.1 mg/kg s.c.) did not affect the anticataleptic effect of idazoxan. The results suggest that idazoxan reversed haloperidol-induced catalepsy by a mechanism involving blockade of alpha(2)-adrenoceptors and, at least in part, 5-HT neurons.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1996

Catalepsy tests: what do they tell us?

In a survey of 200 clinicians regarding their use of catalepsy tests, three fourths of the respondents indicated that they used these tests. In light of this response, and considering both the scientific importance of being able to identify the presence of hypnosis and the fact that catalepsy may account for up to eight of the other indications of hypnosis in use, it is relevant to inquire into the reliability and validity of catalepsy tests. It was found that of the three tests of catalepsy currently in use, only one has the potential for being a test of hypnosis proper and can also justifiably be said to be "of catalepsy." This one test, however, has many serious weaknesses that need to be eliminated if it is to be truly useful.

Catalepsy↗
PubMed1999

Haloperidol-induced within-session response decrement patterns and catalepsy in rats: behavioural dissociation.

The typical antipsychotic haloperidol is known to induce extra-pyramidal side-effects (EPS). Catalepsy in rats is generally regarded as a valid model for detecting the EPS liability of compounds in humans. Together with its antipsychotic and cataleptogenic actions, haloperidol causes an attenuation of instrumental responding which becomes larger in the course of a session: a within-session response decrement. The present study compared the time-course of haloperidol-induced catalepsy, measured by a bar test, to the haloperidol-induced within-session response decrements, measured by operant behaviour under a fixed ratio 10 schedule of reinforcement. Rats were trained to press a lever on a Fixed Ratio 10 schedule of food reinforcement during sessions of 15 min. When responding was stable, saline or haloperidol in 0.03 mg/kg, 0.1 mg/kg, or 0.3 mg/kg was administered intra-peritoneally either 30, 90 or 180 min prior to behavioural testing. The number of lever presses, food tray visits and latency to press the lever and to visit the food tray were analysed in five successive blocks of 3 min. Catalepsy was tested 30, 60, 90, 120, and 180 min. after injection, by placing a rat with its forepaws on a horizontal bar. The latency to remove both forepaws from the bar was scored. Within-session response decrements were present at 0.1 mg/kg and at 0.3 mg/kg, from 30 min after administration onward. At these doses, latency to press the lever was increased after 30 and 90 min, but not significantly after 180 min. Latency to visit the tray was affected only after 30 min, at 0.3 mg/kg. Haloperidol induced a dose-dependent increase in catalepsy from 60 min onwards, with maximal effect after 120 min. A dissociation between the time-course of occurrence of within-session response decrement and the cataleptogenic action of haloperidol, as well as between the latter and both latency measures, was found. Consequently, the present data suggest that within-session response decrements are not obviously caused by catalepsy-related impairments.

Animals↗
PubMed1996

Prevention by (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin of both catalepsy and the rises in rat striatal dopamine metabolism caused by haloperidol.

1. The influence of (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on haloperidol-induced increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxyphenylacetic acid (HVA), was measured in three microdissected brain regions of the rat following a quantitative assessment of catalepsy. 2. Haloperidol alone (2.66 mumol kg-1, i.p.) caused a robust cataleptic response. Given 30 min after haloperidol, 8-OH-DPAT (76 or 760 nmol kg-1, s.c.) prevented catalepsy in 30% and 100% of rats, respectively. 3. Haloperidol significantly increased the DOPAC (by 2 to 4 fold) and HVA (by 3 to 7 fold) contents of the caudate-putamen, nucleus accumbens and medial prefrontal cortex. Given alone, only the lower dose of 8-OH-DPAT caused a significant biochemical change, a doubling of cortical DOPAC. 4. In the cases where catalepsy was prevented by either dose of 8-OH-DPAT, the haloperidol-induced increases in DOPAC and HVA were consistently lower in the caudate-putamen. This pattern was true for the rise in cortical HVA but only in response to the lower dose of 8-OH-DPAT. In contrast, neither dose of 8-OH-DPAT was able to influence the haloperidol-induced rises in cortical DOPAC. In the nucleus accumbens, 8-OH-DPAT did not affect the haloperidol-induced increases in the dopamine metabolites, irrespective of the dose employed or the resulting behaviour. When catalepsy was not prevented, 8-OH-DPAT did not alter the neurochemical responses to haloperidol in any region. 5. These results suggest that part of the mechanism by which 8-OH-DPAT prevents haloperidol-induced catalepsy is reflected by a reversal of the compensatory increase in meso-striatal and/or meso-cortical dopamine neuronal activity that normally accompanies postsynaptic dopamine receptor blockade with haloperidol.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Nicotine potentiates sulpiride-induced catalepsy in mice.

The effects of nicotine on sulpiride-induced catalepsy in mice were investigated. Sulpiride (12.5-100 mg/kg) induced a low degree of catalepsy in mice which was dose dependent. Nicotine (0.0001-1 mg/kg) caused an even lower degree of catalepsy. When the drugs were co-administered a much higher cataleptogenic response was obtained. The potentiation of the effect of sulpiride by nicotine was elicited by 0.5 mg/kg or higher doses of the drug. The central nicotinic receptor antagonist mecamylamine (1-3 mg/kg) and the peripheral antagonist hexamethonium (5 and 10 mg/kg) decreased the response induced by the combination of nicotine and sulpiride. Higher doses of the cholinoceptor antagonist atropine (10 mg/kg) also reduced the catalepsy induced by the drug combination. It is concluded that nicotine potentiates sulpiride-induced catalepsy through activation of cholinergic mechanism(s) and that the central nicotinic mechanism mediates nicotine's action.

Animals↗
PubMed1988

[Emetic and catalepsy-inducing actions of buflomedil].

The emetic and catalepsy-inducing actions of buflomedil were studied in dog and mice. Oral administration of buflomedil (10-30 mg/kg) dose-dependently induced vomiting in dogs. On the other hand, the buflomedil-induced vomiting was inhibited by the pretreatment with domperidone (1 mg/kg, p.o.). A high dose of buflomedil (120-360 mg/kg, p.o.) induced catalepsy in mice, while a low dose of this agent (30-120 mg/kg, p.o.) had no enhancing effect on haloperidol-induced catalepsy. It was also found that the buflomedil-induced catalepsy was inhibited by the pretreatments with L-DOPA (300 mg/kg, i.p.) and bromocriptine (5 mg/kg, i.p.), respectively. These results suggest that buflomedil may induce emetic action as a dopamine agonist at a low dose, whereas it acts as a dopamine antagonist and a catalepsy inducer at a high concentration.

Administration, Oral↗
PubMed2004

Quercetin, a bioflavonoid, reverses haloperidol-induced catalepsy.

Neuroleptics are extensively used in the treatment of schizophrenia and other affective disorders. Unfortunately their use is often associated with distressing side effects involving the extrapyramidal tract, such as Parkinsonism and tardive dyskinesia. Neuroleptic-induced catalepsy has long been used as a model for extrapyramidal side effects such as Parkinsonian-like bradykinesia associated with antipsychotic use in humans. In the present study, haloperidol (2 mg/kg i.p.) was administered to mice to induce catalepsy and cataleptic response was measured for the next 4 h at 1 h intervals. Haloperidol treatment in mice induced a strong cataleptic state within 1 h of injection, reaching a maximal plateau after 2 h and lasting for 4 h. Vehicle-treated animals did not display catalepsy as they remained less than 5 sec on the bar at each time point. Pretreatment with quercetin dose-dependently (25-100 mg/kg p.o.) reduced the catalepsy score in haloperidol-treated animals. A dose response study of quercetin showed a characteristic U-shaped response curve, with maximum suppression observed at a dose of 100 mg/kg. On increasing the dose of quercetin to 300 mg/kg, no statistically significant difference in catalepsy score was observed compared with the haloperidol-treated group. In conclusion, the findings of the present study strongly suggest that quercetin can be screened as a potential drug candidate or as an adjuvant for the treatment of neuroleptic-induced extrapyramidal side effects.

Animals↗