Body pinch induces long lasting cataleptic like immobility in mice: Behavioral characterization and the effect of naloxone

Amir, Shimon; Brown, Zavie W.; Amit, Zalman; Ornstein, Kurt

doi:10.1016/0024-3205(81)90697-4

Cited by 70 publications

(22 citation statements)

References 25 publications

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“…The fact that drug-free or placebo-treated mice and rats, when placed repeatedly on a bar with an imposed posture, "learn" to maintain, even during long periods of time, such posture has been previously reported in some studies (Sanberg et al 1988;Brown and Handley 1980;Amir et al 1981;Ferré et al 1990). According to Ferré et al (1990), the most probable cause of this repeated testing effect is the animal's avoidance of manipulation when both forepaws touch the floor, being well-known that handling is a stressor (Axelrod and Reisine 1984).…”

Section: Discussionmentioning

confidence: 80%

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Chinen

Frussa‐Filho

1999

Neuropsychopharmacology

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The cataleptic behavior induced by the dopamine D 1 antagonist SCH 23390 (SCH) has proven to be a useful assay for investigating the sensitivity of D 1 -like dopamine receptor-mediated effects during chronic drug administration. A fundamental flaw in most of these studies may be the involvement of the "repeated measures effect," a behavioral phenomenon well demonstrated for neurolepticinduced catalepsy but not yet investigated for dopamineThe ability of chronic neuroleptic treatment to produce increasing or decreasing degrees of both Parkinsonism in humans (see Hansen and Hoffman 1997) and catalepsy in laboratory animals (Barnes et al. 1990) over time remains controversial. Specifically, concerning the evolution of catalepsy during chronic haloperidol treatment, tolerance (Asper et al. 1973;Ezrin-Waters and Seeman 1977;Campbell and Baldessarini 1981), sensitization (Antelman et al. 1986;Kinon and Kane 1989;Barnes et al. 1990), or no effects (György et al. 1969;Moller Nielsen et al. 1974;Frussa-Filho et al. 1992) have been reported. Although the patterns of change in catalepsy responses to chronic neuroleptic treatment are influenced by multiple determinants (Barnes et al. 1990), two specific biological mechanisms seem to be of particular importance in determining the development of tolerance or sensitization: dopamine receptor supersensitivity (Ezrin-Waters and Seeman 1977;Hoffman and Beninger 1988) and a learning process due to repeated testing in the catalepsy apparatus (Iwata et al. 1989;Ferré et al. 1990), respectively. In regards to the learning process, both repeated measures in a single session after acute haloperidol administration (Stanley and Glick 1976;Hillegaart et al. 1987 Received October 12, 1998; revised April 30, 1999; accepted May 17, 1999. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 5 Conditioning and SCH 23390-Induced Catalepsy 671 et al. 1990) have been reported to markedly enhance the cataleptic behavior presented by rodents.For many years, dopamine D 2 -like receptors were implicated as the only site mediating the cataleptic behavior of neuroleptics (Seeman 1980). However, in 1984, Christensen et al. (1984 first reported the cataleptogenic properties of SCH 23390, a selective antagonist of D 1 -like dopamine receptors (Hyttel 1983). Thus, besides providing a functional correlate of dopamine D 1 receptor antagonism (Mizuki et al. 1996), SCH 23390-induced catalepsy has proven to be a useful assay for investigating the functional interactions between D 1 -and D 2 -like dopamine receptors (see Klemm 1993). Catalepsy has also been used to investigate the sensitivity of D 1 -like dopamine receptor-mediated effects during chronic drug administration. In two landmark investigations, Hess et al. (1986Hess et al. ( , 1988 reported that although chronic treatment of rats with SCH 23390 resulted in an increase in D 1 -like striatal dopamine receptors as well as in spontaneous locomotion and D 1 -like and D 2 -like dopamine agonist-induced stereotypy, no tolerance to the cataleptic effect ...

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Section: Discussionmentioning

confidence: 80%

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Chinen

Frussa‐Filho

1999

Neuropsychopharmacology

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“…The trial was repeated every 20 s until the rat became motionless in the imposed posture for a criterion duration of 20 s. The number of trials needed to reach the criterion was recorded for each rat. The method stems from Amir et al (1981) and has been used by others (Klemm 1983a, b). RIC was scored till the number of trials for any treatment group came down and then rose to eight or above.…”

Section: Methodsmentioning

confidence: 99%

Prolonged cataleptogenic effects of potentized homoeopathic drugs

1986

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The four homoeopathic drugs, Gelsemium, Cannabis Indica, Graphites and Agaricus Muscarius, administered orally in 30th and 200th potencies on white rats, enhanced restraint-induced catalepsy in a similar manner to the two standard drugs pilocarpine and haloperidol (IP injection at 5 mg/kg). All the drugs tested differed from each other in the duration of cataleptogenic effect, which was more prolonged with Cannabis, Graphites and Agaricus than with Gelsemium and the two non-homoeopathic drugs used. The 200th potency of any homoeopathic drug tested acted longer than its 30th potency.

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“…In previous work on experimental catalepsy, using the 'pinchinduced' model in mice (Amir et al 1981), evidence for a major influence of central cholinergic neutrotransmission was found (Klemm 1983).…”

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confidence: 96%

“…Although it has been argued that pain per se promotes this catalepsy (Ornstein 1981), it has been shown that pain is definitely not involved in a related, Offprint requests to: W. Klemm and perhaps an identical phenomenon known as 'animal hypnosis' (Klemm 1977). …”

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confidence: 98%

Cholinergic-dopaminergic interactions in experimental catalepsy

Klemm

1983

Psychopharmacology

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The 'pinch-induced' model of catalepsy in the mouse was disrupted by atropine sulfate (4 mg/kg IP), confirming an earlier finding, and also by the antinicotinic mecamylamine (4 mg/kg). Either anticholinergic, when given concurrently with haloperidol (5 mg/kg), interfered with the typical haloperidol-induced enhancement of catalepsy. In mice pretreated with a peripheral cholinergic blocker, the cholinomimetic pilocarpine (10 mg/kg) enhanced catalepsy. The dopamine (DA) agonist apomorphine (5 mg/kg) reversed the enhancement that was normally caused by pilocarpine. Apomorphine did not stimulate open field locomotion in mice that were pretreated with pilocarpine. This lack of correlation between catalepsy and open field activity indicates that catalepsy in a unique state that involves more than mere absence of movement. The DA mechanisms, thus, appear to be specifically antagonistic to catalepsy or, conversely, cholinergic mediation of catalepsy involves reduced influence of DA systems.

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Body pinch induces long lasting cataleptic like immobility in mice: Behavioral characterization and the effect of naloxone

Cited by 70 publications

References 25 publications

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Conditioning to Injection Procedures and Repeated Testing Increase SCH 23390-Induced Catalepsy in Mice

Prolonged cataleptogenic effects of potentized homoeopathic drugs

Cholinergic-dopaminergic interactions in experimental catalepsy

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