Is there a relationship between the involvement of extrapyramidal and mesolimbic brain areas with the cataleptic action of neuroleptic agents and their clinical antipsychotic effect?

Costall, B.; Naylor, R.J.

doi:10.1007/bf00428687

Cited by 47 publications

(8 citation statements)

References 9 publications

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“…The latter drugs are known to block central dopamine receptors (Anden et al, 1970) and therefore frequently produce Parkinsonism when administered chronically (Hornykiewicz, 1973). The fact that metoclopramide, like the phenothiazines and butyrophenones, produces catalepsy (Costall and Naylor, 1973) and antagonizes the behavioural effects of apomorphine and amphetamine in laboratory animals (Janssen et al, 1967;Hackman et al, 1973;Dolphin et al, 1975) indicates that it, too, may block dopamine receptors important for motor function as well as those involved in vomiting mechanisms (Peng, 1963).…”

Section: Metoclopramide (4-amino-5-chloro-n-[2-(diethylamino)ethyl]-omentioning

confidence: 99%

Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias.

Tarsy¹,

Parkes²,

Marsden³

1975

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Metoclopramide (4-amino-5-chloro-n-[2-(diethylamino)ethyl]-omentioning

confidence: 99%

Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias.

Tarsy¹,

Parkes²,

Marsden³

1975

Journal of Neurology, Neurosurgery & Psychiatry

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“…Activities against apomorphine-induced climbing and amphetamine-induced locomotion are associated with clinical antipsychotic action, whereas cataleptogenic activity is associated with clinical extrapyramidal side effects (Costall and Naylor 1973;Costall et al 1978;Jenner et al 1978;Jenner and Marsden 1979). Different anatomical sites may be involved in these behaviours.…”

Section: Discussionmentioning

confidence: 99%

The selective dopamine antagonist properties of BRL 34778: a novel substituted benzamide

et al. 1988

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BRL 34778, exo-4-amino-5-chloro-2-methoxy-N-[9-(4-fluorophenylmethyl)-9-azabi cyclo(3.3.1) non-3-yl]-benzamide, is a very potent and specific dopamine D2-receptor antagonist. It exhibits a Ki value of 2.14 nM for dopamine D2-receptors but much lower affinity for D1-(Ki 5700 nM) and for many other receptor types. Its action is potent and of long duration in models for antipsychotic activity (4 h ED50s PO are 0.017 mg/kg for antagonism of apomorphine-induced climbing in mice and 0.028 mg/kg for antagonism of amphetamine-induced locomotion in rats). In contrast to its high potency in models for antipsychotic activity, BRL 34778 is much weaker in models for extrapyramidal effects and sedation (4 h ED50s PO are 2.4 mg/kg for inducing catalepsy in rats and 1.14 mg/kg for inhibition of rearing behaviour in rats). These data indicate potent activity of BRL 34778 in models for antipsychotic activity but low activity in models for extrapyramidal effects and sedation.

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“…Iversen, Reynolds and Snyder (1983 ) write that" the mediation of neuroleptic therapeutic effects by dopamine receptor blockade is probably as well established as is the mediation of any other group (Seeman and Lee 1975;Wyatt 1976;Seeman 1977;Rotrosen et al 1978;Stanley et al 1980;Martindale 1982) is expressed as gmole/day. Vertical axes represent the following measures: A ICso for displacement of binding of [3H] Haloperidol to rat striatal tissue (riM) (Hyttel 1978;Leysen et al 1978a, b); B EDso for increase in rat striatal homovanillic acid levels (pmole/kg) (Lippmann et al 1975;Rollema et al 1976;Scatton et al 1977;Westerink et al 1977;Stanley et al 1980;Dubinsky et al 1982); (2 EDso for production of catalepsy in rats (gmole/kg) (Dnbinsky et al 1982;Niemegeers 1974;Costall and Naylor 1973;Costall and Naylor 1975); D EDso for inhibition of lateral hypothalamic self-stimulation in rat (gmole/kg) (Niemegeers 1974;Wauquier 1979;Schaefer and Michael 1980;Hori et al 1983); 1~ EDs o for inhibition of stereotypy in rats induced by 10 mg/kg amphetamine (gmole/kg) (Wauquier of drugs in psychiatry, or for that matter in general medicine".…”

Section: The Dopamine Hypothesis Of Neuroleptic Actionmentioning

confidence: 99%

The time course of neuroleptic therapy for psychosis: role of learning processes and implications for concepts of psychotic illness

Miller

1987

Psychopharmacology

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In neuroleptic therapy for psychotic illness, clinical improvement is produced more slowly than is central dopamine blockade, and its time course is highly variable between patients. A theory of neuroleptic-responsive psychotic illness thus requires more than dopamine blockade, though that appears to be the first step in the therapeutic process. Some previous explanations given for the protracted time course of neuroleptic therapy are discussed, with emphasis on the hypothesis of delayed inactivation of midbrain dopamine neurones. For various reasons all explanations are unsatisfactory. An alternative hypothesis is proposed in which neuroleptic-responsive psychoses are seen as arising from a hyperactivity of the associations of thought. Such psychoses thus involve a disorder of a high-level learning process, namely the elaboration of memories of thoughts and beliefs. Neuroleptic drugs are envisaged to remedy this process, but not to eradicate the abnormal memories already formed. Psychotic symptoms may thus outlast the start of neuroleptic therapy by many weeks. It is suggested that the pharmacological characteristics of the hypothetical learning process involved in generating psychotic symptoms are analogous to those of a simpler learning process, defineable in animal experiments - namely, the reward component in instrumental conditioning. A preliminary case is made that the relative potency of different neuroleptic drugs in antipsychotic therapy can better be predicted by their relative potency in retarding such a variety of learning, than by other behavioural tests of these drugs.

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Is there a relationship between the involvement of extrapyramidal and mesolimbic brain areas with the cataleptic action of neuroleptic agents and their clinical antipsychotic effect?

Cited by 47 publications

References 9 publications

Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias.

Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias.

The selective dopamine antagonist properties of BRL 34778: a novel substituted benzamide

The time course of neuroleptic therapy for psychosis: role of learning processes and implications for concepts of psychotic illness

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