Disease relevance of Hpic1

• Haloperidol induced catalepsy and muscle rigidity in the control mice, but these responses were significantly reduced in Fyn-deficient mice [1].
• SSR181507 did not induce catalepsy in rats (MED>60 mg/kg i.p.) and antagonized (3-10 mg/kg i.p.) haloperidol-induced catalepsy [2].
• Racemic N-propargyl-1-aminoindan (AGN-1135), besides being of lower potency, had a different dose-dependency than rasagiline in antagonizing haloperidol-induced catalepsy or alpha-MpT-induced hypokinesia [3].
• Since it has been reported that manidipine can worsen parkinsonian symptoms in a patient with Parkinson's disease, we have evaluated catalepsy in manidipine-treated mice and compared this with flunarizine-and haloperidol-induced catalepsy [4].

Psychiatry related information on Hpic1

• These studies were carried out using the spontaneous motor activity (SMA), amphetamine-induced hyperactivity and stereotyped behaviour, pentobarbital-induced hypnosis and exploratory activity, apomorphine-induced climbing and haloperidol-induced catalepsy in rats [5].
• Acute exposure to catnip increased stereotyped behavior and susceptibility to seizures, did not interfere with haloperidol-induced catalepsy, and decreased sleeping time after sodium pentobarbital administration [6].
• The test material was studied for its effect on pentobarbitone hypnosis, motor co-ordination, tail-withdrawal reaction time, electroshock, chemoconvulsions, haloperidol-induced catalepsy and conditioned avoidance response [7].

High impact information on Hpic1

• We conclude that NT is required for haloperidol-elicited activation of a specific population of striatal neurons but not haloperidol-induced catalepsy [8].
• In this study, we explored the role of Fyn in haloperidol-induced catalepsy, an animal model of the extrapyramidal side effects of antipsychotics [1].
• NGFI-B knockout (KO) mice display a profound alteration of haloperidol-induced catalepsy and striatal neuropeptide gene expression [9].
• The haloperidol effects on Fos-li neurons were examined over the range of 0.1 to 6.0 mg/kg; the ED50s for haloperidol-induced catalepsy are 0.4 and 3.8 mg/kg in the D2 and B6 strains, respectively [10].
• In rats, papaverine potentiates haloperidol-induced catalepsy, consistent with the hypothesis that inhibition of PDE10A can increase striatal output and prompting a further evaluation of papaverine in models predictive of antipsychotic activity [11].

Chemical compound and disease context of Hpic1

• 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 [12].
• Morphine-induced catalepsy was enhanced by fenfluramine and attenuated by metergoline, whereas neither fenfluramine nor metergoline had any effect on haloperidol-induced catalepsy [13].
• 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 [14].
• 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 [13].
• These results indicate that co-administration with L-DOPA + carbidopa and single treatment with bromocriptine can decrease haloperidol-induced catalepsy and bradykinesia in mice [15].

Biological context of Hpic1

• Detection and mapping of quantitative trait loci for haloperidol-induced catalepsy in a C57BL/6J x DBA/2J F2 intercross [16].
• For haloperidol-induced catalepsy, significant QTLs were detected on chromosome 14 (two different QTLs) in the CxLP intercross, and chromosomes 1 and 9 in the B6xD2 intercross [17].
• A genome-wide scan was conducted in two F(2) intercrosses, C57BL/6J (B6)xDBA/2J (D2) and BALB/cJ (C)xLP/J (LP), for three different phenotypes: basal locomotor activity, ethanol-induced locomotor activity, and haloperidol-induced catalepsy [17].
• Further studies on the relationship between dopamine cell density and haloperidol-induced catalepsy [18].
• Genetics, haloperidol-induced catalepsy and haloperidol-induced changes in acoustic startle and prepulse inhibition [19].

Anatomical context of Hpic1

• Previous data have suggested that the genetic variability in the sensitivity to haloperidol-induced catalepsy is associated with the number of dopamine neurons in the substantia nigra zona compacta (SNZc) [18].
• The interaction between GABAergic and dopaminergic systems within the central nervous system was investigated in rats using the open-field apparatus and apomorphine-induced stereotypy, and in mice using haloperidol-induced catalepsy [20].

Associations of Hpic1 with chemical compounds

• A muscarinic receptor blocker, atropine, disrupted haloperidol-induced catalepsy [21].
• Haloperidol-induced catalepsy was apparently more easily antagonized by dexamphetamine than by GK 13 or GBR 12783 [22].
• SR 95191 p.o. antagonized the effects of reserpine in mice and rats, decreased immobility in the mouse despair test, antagonized haloperidol-induced catalepsy in rats and potentiated 5-hydroxytryptophan in mice and rats with an overall potency which was half that of imipramine [23].
• In haloperidol-induced catalepsy in rats (1.5 mg/kg, s.c.) or mice (4-6 mg/kg s.c.), rasagiline improved recovery of normal locomotion, gait and coordination at 0.4-2.4 mg/kg i.p. and 1.8-1.5 mg/kg i.p., respectively [3].
• Oral ST 1535, at 1.25 and 2.5 mg/kg, potentiates L-dopa effects in reducing haloperidol-induced catalepsy [24].

Regulatory relationships of Hpic1

• Moreover, glucagon inhibited the locomotor and exploratory activity as well as the amphetamine-induced hyperactivity and enhanced haloperidol-induced catalepsy [25].

Other interactions of Hpic1

• Differential effects of cyclooxygenase inhibitors on haloperidol-induced catalepsy [26].

Analytical, diagnostic and therapeutic context of Hpic1

• CM 30366 induced stereotyped behaviour and antagonized haloperidol-induced catalepsy in rats, after parenteral and oral administration [27].
• D2 DA receptor autoradiography was performed using 125I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025] [28].
• 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) [29].
• Fenvalerate at 15, 30 and 45 mg/kg dose increased start latency, decreased ambulation and rearing in open-field, increased immobility in tail-suspension test and attenuated haloperidol-induced catalepsy in a dose-dependent manner [30].

References