Disease relevance of Catalepsy

• Haloperidol, a widely used antipsychotic drug, was tested for its ability to block the behavioral response to amphetamine and to elicit catalepsy in rats treated with saline or ascorbic acid (1000 milligrams per kilogram of body weight) [1].
• Here we show that mice lacking the enzyme fatty acid amide hydrolase (FAAH(-/-)) are severely impaired in their ability to degrade anandamide and when treated with this compound, exhibit an array of intense CB(1)-dependent behavioral responses, including hypomotility, analgesia, catalepsy, and hypothermia [2].
• We found that the typical antipsychotic raclopride was much less potent in inhibiting locomotor activity and eliciting catalepsy (or parkinsonism) in D2L(-/-) mice, whereas the atypical antipsychotic clozapine was equally effective in D2L(-/-) and wild-type mice [3].
• MPEP (1.0-10mg/kg ip) inhibited the muscle rigidity, electromyographic activity, hypolocomotion and catalepsy induced by haloperidol [4].
• After 17 days of repeated injections, morphine no longer elicited hypokinesia and catalepsy, but no cross-tolerance developed to the AMT behavioral changes [5].

Psychiatry related information on Catalepsy

• To test this hypothesis, the effects of SCH 32615, an enkephalinase inhibitor, on DA antagonist-induced catalepsy, DA D-1 agonist-induced non-stereotyped grooming, and DA D-2 agonist-induced stereotyped behavior were studied [6].
• These results strongly suggest that carteolol improves haloperidol-induced catalepsy via its beta-adrenoceptor antagonistic activity and is expected to be effective in the treatment of akathisia without attenuating neuroleptic-induced antipsychotic effects due to its postsynaptic dopamine receptor antagonistic activity [7].
• Nitric oxide synthase (NOS) inhibitors interfere with motor activity, disrupting rodent exploratory behavior and inducing catalepsy [8].
• IT alfentanil in saline produced a dose-dependent increase in the HP response latency and this effect was accompanied by a similar dose-dependent increase in the incidence of catalepsy and blockade of corneal responses, indicating a rapid supraspinal redistribution [9].
• Like CCK-8, CER and some of its analogues produce many behavioural effects in mammals: inhibition of intake of food and water; antinociception; sedation; catalepsy; ptosis, antistereotypic, anticonvulsive and tremorolytic effects; inhibition of self-stimulation [10].

High impact information on Catalepsy

• Haloperidol-induced catalepsy is mediated by postsynaptic dopamine receptors [11].
• Pavlovian conditional tolerance to haloperidol catalepsy: evidence of dynamic adaptation in the dopaminergic system [12].
• The monolateral microinjection of the [d-Ala2]] analog (3 to 6 micrograms) into the caudate nucleus increased the concentration of dihydroxyphenylacetic acid in the injected side, whereas bilateral injection increased the concentration of this compound in both caudate nuclei and caused catalepsy [13].
• However, we found that catalepsy, which is thought to reflect the EPS of typical APDs, is unaffected in NT-null mutant mice, suggesting that NT does not contribute to the generation of EPS [14].
• By contrast, haloperidol, a typical neuroleptic that acts preferentially at D2-class receptors, remains effective in inducing catalepsy and striatal Fos/Jun expression in the D1 mutants, and these behavioral and neural effects can be blocked by D2 dopamine receptor agonists [15].

Chemical compound and disease context of Catalepsy

• Previous lesion studies have shown that the dopamine receptors in the striatum are involved in this neuroleptic-induced catalepsy [11].
• Dermorphin-related peptides from the skin of Phyllomedusa bicolor and their amidated analogs activate two mu opioid receptor subtypes that modulate antinociception and catalepsy in the rat [16].
• Haloperidol- but not SCH 23390-induced catalepsy was attenuated by intrastriatally administered 7-chlorokynurenate [17].
• Both the NMDA antagonist (-)2-amino-7-phosphonoheptanoate [(-)AP7], and the GABA agonist muscimol, but not the muscarinic antagonist scopolamine, induced catalepsy and limb rigidity [18].
• Both the (-)AP7- and muscimol-induced catalepsy were antagonized by coadministration of NMDA and the GABA antagonist bicuculline [18].

Biological context of Catalepsy

• Consistent with the D(2) KO phenotype, A(2A)R inactivation partially reversed both acute D(2)R antagonist (haloperidol)-induced catalepsy and chronic haloperidol-induced enkephalin mRNA expression [19].
• In pigeons, PK 26124 and mephenesin produced loss of righting that was to some extent associated with eye closure and muscle relaxation, whereas PCP produced catalepsy, i.e., loss of righting without eye closure and without muscle relaxation [20].
• Role of adenosine and N-methyl-D-aspartate receptors in mediating haloperidol-induced gene expression and catalepsy [21].
• Lastly, some dopamine D2 binding sites in the striatum are located on cortico-striatal afferent terminals and blockade of these striatal D2 sites may be involved in the induction of catalepsy by neuroleptic drugs [22].
• Sex differences in catalepsy: evidence for hormone-dependent postural mechanisms in haloperidol-treated rats [23].

Anatomical context of Catalepsy

• Injection of apomorphine into the medial prefrontal cortex of the rat increases haloperidol-induced catalepsy [24].
• Onset of symptoms (severe catalepsy and loss of righting reflex, but before the onset of convulsions) was accompanied by marked decreases of glutamate and glutamine in striatum and hippocampus [25].
• The increased TRGABA in globus pallidus elicited by these opioid receptor agonists may be associated with catalepsy since muscimol, a specific GABA receptor agonist, injected into the globus pallidus causes a dose-related catalepsy [26].
• The local application of 8-OH-DPAT (0.5 or 2.5 micrograms/rat, 10 min) into the median, but not the dorsal, raphe nucleus resulted in a reversal of the catalepsy induced by the DA D2 receptor blocking agent raclopride (16 mg kg-1 s.c., 60 min) [27].
• Since this GABA receptor agonist injected into the substantia nigra fails to cause catalepsy, one can exclude that the increase in the TRGABA of substantia nigra elicited by opiate receptor agonists is operative in mediating the catalepsy elicited by opioids [26].

Gene context of Catalepsy

• Interestingly, catalepsy induced by raclopride, a specific dopamine D(2)/D(3) antagonist is completely abolished in NGFI-B-deficient mice whereas the cataleptic response to SCH 23390, a dopamine D(1) agonist, is preserved [28].
• However, activation of CB1 receptors is also associated with central side effects, including ataxia and catalepsy [29].
• Attenuation of haloperidol-induced catalepsy by a 5-HT2C receptor antagonist [30].
• The selective 5-HT2C/2B receptor antagonist, SB-228357 (0.32-10 mg kg(-1) p.o.) significantly reversed haloperidol-induced catalepsy whereas the 5-HT2A and 5-HT2B receptor antagonists, MDL-100907 (0.003-0.1 mg kg(-1) p.o.) and SB-215505 (0.1-3.2 mg kg(-1) p.o.) respectively did not reverse haloperidol-induced catalepsy [30].
• Pharmacological and pharmacokinetic characterization of the cannabinoid receptor 2 agonist, GW405833, utilizing rodent models of acute and chronic pain, anxiety, ataxia and catalepsy [29].

Analytical, diagnostic and therapeutic context of Catalepsy

• RATIONALE: In animal models of reduced dopamine transmission, such as haloperidol-induced catalepsy or monoamine-depleted animals, serotonin (5-hydroxytryptamine; 5-HT) 5-HT(1A) agonists appear to enhance motor activity [31].
• The reductions in the duration of catalepsy and decreases in striatal ACh release associated with CP-99,994 perfusion were positively correlated [32].
• Thus, several lines of evidence indicate that the catalepsy induced by neurotensin is not the consequence of the neurotensin induced hypothermia [33].
• The liability of causing extrapyramidal side effects was investigated in models of catalepsy and by high-performance liquid chromatography (HPLC) detection of dopamine turnover in several brain regions [34].
• Intraventricular injection of the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), which caused marked depletion of 5-HT in brain, did not change haloperidol-induced catalepsy per se, but completely antagonized the anticataleptic effect of subcutaneously administered 8-OH-DPAT [35].

References