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PubMed1987

Transient supression by stress of haloperidol induced catalepsy by the activation of the adrenal medulla.

Rats were injected with haloperidol (0.5-1.0 mg X kg-1). When the catalepsy score was almost maximal (60 s, measured by the bar-test), the rats were handled, exposed to cold (3 degrees C) or immobilized. After each of these stress procedures the catalepsy was significantly reduced. Handling of adrenalectomized rats gave no such reduction. Infusion of adrenaline (10 nmol X kg-1, given in 15 s), in contrast to that of isoprenaline and phenylephrine (both the same concentration as adrenaline) also reduced the haloperidol induced catalepsy. These findings indicate that neuroleptic catalepsy in rats is not only mediated through central but also through peripheral mechanisms, e.g. by the adrenal medulla.

Adrenal Medulla↗
PubMed1993

Inheritance of predisposition to catalepsy in mice.

"Pinch-induced" catalepsy (excessive freezing) was studied in mice of nine inbred strains. The CBA/Icg strain had the highest predisposition to catalepsy, with 56% males and 73% females exhibiting 120-s immobility after four tests. A Mendelian analysis of predisposition to catalepsy was performed on CBA/Icg and AKR/J mice contrasting in this trait. Reciprocal F1 hybrids did not display freezing after 10 tests. The number of cataleptic and noncataleptic animals among the F2's and in the families of the CBA x F2 backcrosses agreed with the hypothesis that the pronounced predisposition to catalepsy in the CBA/Icg mice was determined by a single autosomal locus in homozygous recessive condition.

Animals↗
PubMed1992

Evidence for separate neuronal mechanisms for the discriminative stimulus and catalepsy induced by delta 9-THC in the rat.

The cataleptogenic effect of delta 9-THC was compared to its discriminative stimulus effects in rats. The ED50s for the discriminative stimulus and catalepsy were 0.8 and 4.0 mg/kg, respectively, while their time courses were very similar. The ED50 of delta 9-THC for catalepsy in experimentally naive rats was not different from that in rats trained with the drug discrimination procedure, indicating that the cataleptogenic effect was not appreciably attenuated by long-term exposure to low doses of delta 9-THC. Pharmacologically, the catalepsy produced by delta 9-THC more closely resembled that of haloperidol than of morphine, since anticholinergic pretreatment eliminated the delta 9-THC-induced catalepsy while pre-treatment with naloxone had no effect. Although the cataleptogenic effect of delta 9-THC could be pharmacologically manipulated by anticholinergic pre-treatment, its discriminative stimulus effects were not changed in the same animals. These results demonstrate that distinctive mechanisms of action exist for these cannabinoid-induced behaviors.

Animals↗
PubMed1997

Pontine reticular formation is involved in catalepsy produced by cholinergic drugs.

Bilateral kainic acid lesions of the ventro-medial (VM) thalamic nucleus of rats which greatly reduced the catalepsy produced by haloperidol (2 mg/kg i.p.) not only did not reduce, but even enhanced, the cataleptogenic effect of eserine (1 mg/kg i.p.) and arecoline (30 mg/kg i.p.). This finding is in accord with former conclusions that catalepsy produced by cholinergic drugs does not depend on striatal mechanisms. In rats with kainic acid lesions of the VM thalamic nucleus, and similarly in intact, non-lesioned rats, systemic administration of eserine and arecoline potentiated the catalepsy produced by microinjections of carbachol (2 microg) into the pontine reticular formation (PRF). Atropine microinjected bilaterally into the PRF attenuated the cataleptogenic effect of eserine and arecoline i.p. We suggest that the PRF is a site at which systemically given cholinergic drugs act to produce catalepsy.

Animals↗
PubMed1976

Postnatal development of dopaminergic and cholinergic catalepsy in the rat.

The cataleptic response to various doses of the dopamine-receptor antagonist spiperone and the cholinergic agonist pilocarpine was investigated in rats of different ages. Spiperone produced catalepsy in rats 1, 5 and 10 days old, and also in adults. Pilocarpine produced catalepsy in 15- and 20-day old rats, as well as in adults, but not in 10-day old animals. These results suggest that dopaminergic neurons involved in catalepsy are already functional in neonates. Cholinergic substrates of catalepsy, on the other hand, appear to reach functional maturity after the second week of life.

Aging↗
PubMed1991

Striatal N-methyl-D-aspartate receptors in haloperidol-induced catalepsy.

Bilateral ablation of the frontal cortex of rats markedly reduced the catalepsy induced by haloperidol (1 mg/kg i.p.). Similarly, the selective antagonist of N-methyl-D-aspartate (NMDA) receptors, D(-)-2-amino-5-phosphonopentanoic acid (10 micrograms/side), injected bilaterally into the rostral part of the caudate-putamen (CP) reduced haloperidol-induced catalepsy whereas its injection into the intermediate part of the CP was ineffective. The quisqualate receptor antagonist, L-glutamic acid diethyl ester (100 micrograms/side), did not affect haloperidol-induced catalepsy when injected into the rostral part of the CP. On the other hand, NMDA (1 micrograms/side) injected bilaterally into the rostral part of the CP was able to restore haloperidol-induced catalepsy in frontally decorticated rats without any notable cataleptic effect of its own. These findings suggest that a certain degree of tonic stimulatory effect of corticostriatal glutamatergic pathways on NMDA receptors within the rostral part of the CP is a prerequisite for the expression of the cataleptogenic action of haloperidol.

Animals↗
PubMed1993

NMDA receptor antagonists inhibit catalepsy induced by either dopamine D1 or D2 receptor antagonists.

In the present study, we investigated the ability of NMDA receptor antagonists to inhibit catalepsy induced by haloperidol, or SCH23390 and clebopride, selective dopamine D1 and D2 receptor antagonists respectively. Catalepsy was measured by recording the time the animal remained with its forepaws placed over a rod 6 cm above the bench. Pretreatment with either the non-competitive NMDA receptor antagonist, MK-801 (0.25-0.5 mg/kg i.p.) or the competitive antagonist, LY274614 (10-20 mg/kg i.p.) reduced the cataleptic response produced by haloperidol (10 mg/kg), SCH23390 (2.5-10 mg/kp i.p.) or clebopride (5-20 mg/kg i.p.). This demonstrates that NMDA receptor antagonists will reduce both dopamine D1 and D2 receptor antagonist-induced catalepsy. Muscle relaxant doses of chlordiazepoxide (10 mg/kg i.p.) failed to reduce the catalepsy induced by haloperidol, suggesting that the anticataleptic effect of the NMDA receptor antagonists was not due to a non-specific action. These results support the hypothesis that NMDA receptor antagonists may have beneficial effects in disorders involving reduced dopaminergic function, such as Parkinson's disease.

Animals↗
PubMed1983

Alterations in apomorphine concentration in spinal cord and brain follow the time course of catalepsies induced by different treatments.

Because evidence for the neurotransmitter role of dopamine in the gray matter of the spinal cord is accumulating, a question arises of whether or not spinal dopamine receptors are also involved in the effects of dopaminomimetics which are believed to induce beneficial effects in Parkinson's disease through an action thought to be mediated mainly by striatal dopamine receptors. To test this hypothesis muscimol and picrotoxin were injected unilaterally into the posterior part of the substantia nigra of rabbits permanently implanted with stainless-steel cannulae. Muscimol (a GABA-mimetic) enhanced locomotor activity, evoked a stereotyped behavior and contralateral rotations, and increased apomorphine-induced gnawing. Picrotoxin, a substance which inhibits GABA transmission, induced ipsilateral rotations, evoked catalepsy and muscle rigidity, and inhibited locomotor activity. Picrotoxin abolished apomorphine-induced gnawing, and increased haloperidol-mediated catalepsy. The catalepsy induced by an intranigral injection of picrotoxin, and the picrotoxin-evoked blockade of the apomorphine-induced gnawing disappeared within 16 h after the intranigral injection. Alterations in the apomorphine concentration in brain structures (n. caudatus and cerebral cortex) and in spinal cord after picrotoxin injection followed the same time course as the behavioral changes, and returned to the control values 16 h after injection of picrotoxin. Apomorphine was always injected 30 min before the rabbits were killed. Moreover, the substantial increase (to 300%) in apomorphine concentration in the spinal cord probably reflects the antagonism between behavioral changes induced by picrotoxin and the haloperidol catalepsy, rather than the decreased apomorphine concentrations observed in the brain structures. We suggest, therefore, that there exists a correlation between the behavioral effects, which are generally accepted as laboratory models of Parkinson's disease, and the enhanced apomorphine concentration in the spinal cord.

Animals↗
PubMed1990

Role of N-methyl-D-aspartate (NMDA) receptors in experimental catalepsy in rats.

N-methyl-D-aspartic acid (NMDA; 40 mg/kg, i.p.) did not elicit catalepsy, but it potentiated the cataleptic effect of haloperidol and GABAB receptor agonist, baclofen. MK-801 (0.2 mg/kg, i.p.), NMDA-receptor antagonist, reversed haloperidol- but not baclofen-induced catalepsy. MK-801 also potentiated the anticataleptic effect of scopolamine and bromocriptine against haloperidol-induced catalepsy. Dihydropyridine (DHP) calcium-channel antagonists such as nimodipine and nitrendipine (10 mg/kg, i.p.), reversed the anticataleptic effect of MK-801, and potentiated the cataleptic effect of haloperidol, as well as baclofen. These observations indicate the involvement of NMDA receptors in catalepsy, and suggest a potential clinical implication of NMDA-receptor antagonists in Parkinson's disease.

Animals↗
PubMed1989

Comparison of isomers of ketamine on catalepsy in the rat and electrical activity of the brain and behavior in the cat.

The present study compared the relative potency and efficacy of the two isomers of ketamine on the duration of catalepsy (loss of righting reflex) in female rats and on the behavior and electroencephalogram of cats. In the rat, at small doses, the S(+) isomer was more potent than the R(-) isomer or racemic ketamine, while at larger doses, the S(+) isomer and the racemate were equipotent and the R(-) isomer was significantly less potent. Tolerance developed rapidly to the effects of either isomer and both were equally cross-tolerant to racemic ketamine. Sub-effective doses of morphine significantly increased the potency of S(+), R(-) and racemic ketamine on the duration of catalepsy. Sub-effective doses of either isomer augmented the duration of catalepsy, induced by small doses of morphine, but reduced that of large doses. In cats, there was a parallel time course and progression of behavioral and electroencephalographic states in response to equal total doses of either racemic ketamine, an artificial 50:50 mixture of S(+) and R(-) isomers, or the S(+) isomer alone; approximately equivalent effects required twice the dose of the R(-) isomer. It is concluded that there is a common site of action for the two isomers, but there is also a stereospecific difference in potency, as regards the induction of catalepsy in the rat and behavioral and electroencephalographic effects in the cat. Stereospecificity was not apparent in the development of tolerance, cross-tolerance or the augmentation of the response to morphine.

Animals↗
PubMed1993

Partial 6-hydroxydopamine-induced lesions and haloperidol-induced catalepsy.

Rats with partial (36%) 6-hydroxydopamine-induced lesions of the striatal dopamine system or sham-lesioned controls were tested for duration of catalepsy after 1.0, 2.0 and 4.0 mg/kg haloperidol. Thereafter, half of each group was given haloperidol (2.0 mg/kg) chronically for 84 days. The cataleptic responses to the 3 doses were tested again on days 13-15 and 74-76 of the chronic injections. Animals that were lesioned and treated with haloperidol chronically had longer durations of catalepsy at the first two dose-response determinations. At the third dose-response determination, there were no differences among the 4 groups. Additionally, all groups displayed an increase in duration of catalepsy at the second and third dose-response determinations, relative to the first. The increase in haloperidol-induced duration of catalepsy in the lesioned group suggests that lower levels of dopamine in the striatum may potentiate extrapyramidal side-effects.

Aging↗
PubMed1988

Alpha noradrenergic agonists promote catalepsy in the mouse.

Alpha adrenergic receptors are important in motor control. Adrenergic drugs reportedly modulate the catalepsy caused by other agents, such as opiates and neuroleptics. We tested a variety of adrenergic agonists and blockers in a nondrug, mouse model of catalepsy. A major cataleptic effect was produced by both alpha agonists, phenylephrine (0.5 to 3 mg/kg, IP) and clonidine (0.5 to 2 mg/kg), and this catalepsy was antagonized by pretreatment with both of the respective antagonists, phenoxybenzamine (alpha-1) and yohimbine (alpha-2) (p less than 0.0001). The mixed beta agonist, isoproterenol (2 mg/kg), appeared to have a minor cataleptic effect, and this was abolished by beta antagonist. Open-field locomotor scores during the same treatments revealed that catalepsy and hypokinesia are dissociable.

Adrenergic alpha-Agonists↗
PubMed1990

Spinal paralysis and catalepsy induced by intrathecal injection of opioid agonists.

The intrathecal administration of high (1.05 mumol) doses of D-Ala2-Met5-enkephalinamide (DAMA), D-Ala2-Leu5-enkephalinamide (DADLE), Try-D-Thr-Gly-Phe-Leu-Thr, MR2034-TA, dextrorphan tartrate, U50,488H, levorphanol tartrate, methadone hydrochloride, and 1-methyl-4-phenyl-4-propionoxypiperidine induced spinal hypokinesia. The first 5 of these compounds caused spinal paralysis, whereas the other compounds and lower doses of the first 4 induced waxy catalepsy that was restricted to the hindquarters of rats. The paralysis induced by DAMA was not reversible by IT injections of 50 micrograms naltrexone, indicating, together with the paralytic effects of dextrorphan, that traditional opiate receptors are not involved in this behavioral effect. The spinal catalepsy induced by 0.26 mumol of DAMA was prevented by IT pretreatment with 10 micrograms of naltrexone. In view of this finding and the observation that spinal catalepsy can be induced by agonists of all opiate receptor classes, it seems likely that spinal catalepsy is produced by activation of specific opiate receptors, although the subtype remains to be established.

Animals↗
PubMed1992

Upregulation of postsynaptic dopamine receptors in the striatum does not influence haloperidol-induced catalepsy in mice.

The incidence of haloperidol-induced catalepsy was investigated in mice whose postsynaptic dopamine (DA) receptors in the striatum had been upregulated by denervation with 6-hydroxydopamine (6-OHDA). In nonupregulated mice, which were injected with 6-OHDA 4 days before, DA in the striatum fell to 21% of the level found in vehicle-injected mice but [3H]spiperone binding to the membrane of the striatum did not increase. In upregulated mice, which were injected with 6-OHDA 28 days before, DA was at 24% and [3H]spiperone binding increased by 15%. The ED50 values (with 95% confidence limits) for haloperidol-induced catalepsy in nonupregulated mice and that in upregulated mice was 0.40 mg/kg (0.25-0.65 mg/kg) and 0.29 mg/kg (0.16-0.51 mg/kg), respectively. There was no significant difference in the incidence of catalepsy between the two groups of mice. This suggests that the intensity of catalepsy produced by the DA receptor blockade may be unaltered even when the density of receptors increases.

Animals↗
PubMed1992

Quantitation of rodent catalepsy by a computer-imaging technique.

Catalepsy is usually defined as a behavioral state in which an animal maintains an unnatural posture for an extended period of time. While numerous laboratory models have been developed for assessing catalepsy, a common problem encountered with most procedures is the difficulty in quantitating immobility. Measurement of catalepsy is still frequently subjective in nature. To eliminate this subjectivity, a computer-based technique was developed for quantitating catalepsy in mice and rats as measured on the elevated ring. The system consisted of a video camera that was focused on either three mice or two rats. Their behavior was recorded during a 5-min session on videotape that was subsequently transmitted to a Macintosh II microcomputer via a Scion Image-Capture 2 board. A modification of the NIH Image 1.17 public domain program allowed the image of the rat to be transformed to a purely black or white image by assigning pixel values of either 0 or 256. The subsequent captured image was preprocessed in an identical manner and each pixel was subtracted from its corresponding pixel in the previous frame. Thus, changes in animal posture between the two frames can be quantitated. One subtraction cycle (acquisition, bilevel processing, and subtraction) was repeated at an average rate of approximately one per second. To quantitate immobility by image analysis, each frame was subtracted from the previous frame during a 5-min session. The resulting data were sorted according to the magnitude of movement (number of changed pixels) and plotted vs. time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effect of morphine-induced catalepsy, lethality, and analgesia by a benzodiazepine receptor agonist midazolam in the rat.

Previously we have shown that intrathecal administration of midazolam can increase or decrease morphine-induced antinociception, depending upon relative concentration of these drugs by modulating spinal opioid receptors, and it also can inhibit morphine-induced tolerance and dependence in the rat. Now we report that midazolam also influences catalepsy, lethality, and analgesia induced by morphine in the rat. In the acute treatment, animals were first treated with saline or midazolam (0.03 to 30.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (1.0 to 100.0 mg/kg, b.wt., SC). The catalepsy was measured 60 min after the second injection and lethality was checked after 24 h. Midazolam injection increased the morphine-induced catalepsy and lethality. In the chronic treatment, animals were injected with two injections daily for 11 days. The first injection consisted of saline or midazolam (0.03 to 3.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (10.0 mg/kg, b.wt., IP) was given. Lethality, antinociception, and body weight were measured. Chronic morphine treatment also increased lethality in a dose-dependent manner. Chronic treatment with midazolam and morphine increased the antinociception on day 11, as measured in the tail-flick and hot-plate tests. Midazolam administration also prevented the morphine-induced weight loss. These results suggest a strong interaction between midazolam and morphine in altering catalepsy, lethality, and analgesia in rat.

Analgesics↗
PubMed1994

Competitive NMDA antagonists enhance the catalepsy induced by delta 9-tetrahydrocannabinol in mice.

Competitive N-methyl-D-aspartate (NMDA) receptor antagonists, such as CPP and AP-7, dose-dependently enhanced the catalepsy induced by delta 9-tetrahydrocannabinol (THC; 5 mg/kg) in mice, but CPP failed to enhance haloperidol-induced catalepsy. The enhancing effect of CPP on THC-induced catalepsy was dose-dependently blocked by a muscarinic receptor antagonist, scopolamine, and by dopamine D1 and D2 receptor agonists such as apomorphine, SKF 38393 and quinpirole. The effect of CPP was quite opposite to that of the noncompetitive NMDA receptor antagonist MK-801. Therefore, the THC-induced catalepsy model may be useful for distinguishing between both classes of NMDA receptor antagonists.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Tyr-MIF-1 attenuates development of tolerance to spiperone-induced catalepsy in rats.

Because the tripeptide MIF-1 (Pro-Leu-Gly-NH2) is known to attenuate the effects of neuroleptic-induced catalepsy as well as neuroleptic-induced proliferation of dopamine (DA) receptors, we studied the related naturally occurring peptide, Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) for similar properties. Male rats were treated SC for 11 consecutive days with either the DA D1 receptor antagonist SCH 23390 HCl (0.50 mg/kg per day), the DA D2 receptor antagonist spiperone HCl (0.30 mg/kg per day), or vehicle. Half the rats were cotreated daily with Tyr-MIF-1 (1.0 mg/kg per day). The cataleptic effects of SCH 23390 were not altered by Tyr-MIF-1. Tolerance to SCH 23390-induced catalepsy did not develop during the 11-day treatment, and Tyr-MIF-1 had no effect on SCH 23390-induced catalepsy. However, tolerance developed to spiperone-induced catalepsy, and Tyr-MIF-1 attenuated this development of tolerance (p < 0.001). Locomotor and stereotyped activities of the DA D1 and D2 agonists, SKF 39393 (3.0 mg/kg) and quinpirole (3.0 mg/kg) were not affected by Tyr-MIF-1 after treatment with the DA antagonists was discontinued. Tyr-MIF-1 did not alter the Bmax or Kd for in vitro binding of [3H]SCH 23390 and [3H]spiperone to homogenates of the striatum. These findings indicate that Tyr-MIF-1 is able to selectively affect the development of receptor tolerance to a DA D2 receptor antagonist, and that this effect is unrelated to changes in affinity or numbers of D2 receptors.

Amino Acid Sequence↗