Decrease in rat striatal acetylcholine levels by some direct- and indirect-acting dopaminergic antagonists

Consolo, S.; Ladinsky, H.; Bianchi, S.

doi:10.1016/0014-2999(75)90179-x

Cited by 54 publications

(9 citation statements)

References 24 publications

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“…The effects on ACh release were very much attenuated in the nucleus accumbens which is consistent with earlier studies where both dopamine agonists and neuroleptics have little effect on ACh release and turnover compared to the striatum (Bartbolini et aL, 1976;Consolo et aL, 1975;de Bellerocbe and Neal, 1982;. The similar inhibitory effect of the ergot derivatives to apomorphine and dopamine (Miller and Frkdboff, 1979;de Bellerocbe et aL, 1982) indicates that the action is unlikely to be mediated through the activation of adenylcyclase since bromocriptine and lergotrile inhibit the striatal dopamine-stimulated adenylcyclase.…”

Section: Action Of Dopamine Agonists On Dcetylcboline Releasesupporting

confidence: 90%

“…haloperidol and clozapine, turnover being increased in nucleus accumbens but unaffected in corpus striatum (Marco et aL, 1976). This contrasts with the effects of neuroleptics on acetylcholine turnover where a preferential stimulation of turnover is obtained in striatum (Consolo et aL, 1975;Mao et al, 1977) and indicates a different organization of neurone types in these regions.…”

Section: Introductionmentioning

confidence: 55%

“…Results obtained using this method have been shown to parallel those obtained in vivo, for example, a clear inhibitory action of dopaminergic agonists on cholinergic neurones in the striatum has been demonstrated in vitro (de Belleroche and Neal, 1982; de as occurs when release and turnover are measured in vivo (Consolo et al, 1975;Bartholini et al, 1976). In this study, we have used agents which have a selective action at dopamine receptors not linked to adenylcyclase, bromocriptine and lergotrile, to further characterize the receptor mediating the effects of dopamine on GABA and ace@choline release.…”

Section: Introductionmentioning

confidence: 58%

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Action of apomorphine, bromocriptine and lergotrile onγ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

Belleroche

Gardiner

1983

J. Neural Transmission

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The effect of three dopamine agonists, apomorphine, bromocriptine and lergotrile, was tested on the release of gamma-aminobutyric acid, (GABA) and acetylcholine (ACh) from tissue slices of rat nucleus accumbens and striatum. All three agents in vitro caused a dose dependent depression of the K+-evoked release of [14C]-GABA in corpus striatum. This effect was also obtained following in vivo drug application and when endogenous GABA release was determined. A similar depression of GABA release was obtained in the nucleus accumbens. Both dopamine and dibutyryl adenosine-3':5'-cyclic monophosphoric acid inhibited the K+-evoked release of [14C]-GABA in corpus striatum. This inhibitory effect was not reversed by sulpiride. Bromocriptine and lergotrile also depressed the K+-evoked release of [3H]-acetylcholine from tissue slices of corpus striatum but not nucleus accumbens, as has previously been demonstrated for dopamine and apomorphine. In contrast, sulpiride enhanced the release of [3H]-acetylcholine and molindone reversed the apomorphine inhibition of [3H]-acetylcholine release. These results indicate that dopaminergic agents may influence the release of both GABA and ACh in the corpus striatum but only GABA in the nucleus accumbens.

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Section: Action Of Dopamine Agonists On Dcetylcboline Releasesupporting

confidence: 90%

Section: Introductionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 58%

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Action of apomorphine, bromocriptine and lergotrile onγ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

Belleroche

Gardiner

1983

J. Neural Transmission

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“…It is well known that catalepsy is induced not only by drugs which decrease the dopaminergic transmission but also by the cholinomimetic drugs. The nigrostriatal dopaminergic neurons exert a direct inhibitory influence on the activity of striatal cholinergic neurons (14)(15)(16). As to the mecha nism of catalepsy, the simplest interpretation is that the catalepsy is induced by the direct stimulation of cholinergic receptors with chilonomimetics or by the excitation of cholinergic neurons through the blockade of inhibitory activity of dopaminergic neurons with neuro leptics.…”

Section: Discussionmentioning

confidence: 99%

Effects of Bilateral Lesions in the Striatum or Nucleus Accumbens on the Cataleptogenic Activity of Neuroleptics in Rats

Honma

Fukushima

1978

Japanese Journal of Pharmacology

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Abstract-To investigate the role of the striatum and nucleus accumbens in neuroleptic induced catalepsy, bilateral electrocoagulations were made or microinjections of 6-hydroxydopamine (6-OHDA) were given to rats in these brain regions, and the cata leptogenic activity of neuroleptics was measured. Electrocoagulation in these regions caused a highly specific destruction of brain tissue, and 6-OHDA decreased the levels of dopamine in the injected region with little effect on these levels in other regions. The cataleptogenic activity of haloperidol was enhanced by the electrocoagulation in the striatum at 2 days after the operation, but was weakened from 7 days on. The elec trocoagulation weakened the catalepsy induced by chlorpromazine, thioridazine, and ID-4708 (a new butyrophenone derivative), but enhanced that by clozapine at 2 weeks after the operation.Microinjection of 6-OHDA into the striatum enhanced the catalepsy induced by the five neuroleptics used. The lesions in the nucleus accum bens had fewer effects on catalepsy than did those in the striatum. It was concluded that the striatum more than the nucleus accumbens is involved in producing cata lepsy with neuroleptics, and that the enhancement of catalepsy by electrocoagula tion in the striatum is characteristic of clozapine.Pharmacological, biochemical and electrophysiological investigations showed that neuroleptics block dopamine (DA) receptors in the brain (1-3). Almost all neuroleptics produce catalepsy in rats. Reserpine and tetrabenazine reduce the monoamine contents and produce catalepsy (4, 5). These facts suggest that the catalepsy is the result of blockade of DA receptors or the reduction of the activity of DA neurons (6). DA containing nerve terminals are localized in the striatum and nucleus accumbens (7). Therefore, the catalepsy may be induced by the effect of drugs on these brain regions. The present study was under taken to investigate the contribution of DA neurons in the striatum (extrapyramidal system) and nucleus accumbens (mesolimbic system) to the catalepsy induced by neuroleptics.There are data as to the effects of electrocoagulation in the caudate-putamen on the catalep togenic activity of several neuroleptics (8, 9). We investigated the effects of electrocoagu lation in the striatum or nucleus accumbens on the cataleptogenic activity of haloperidol, ID-4708 (a new butyrophenone derivative), chlorpromazine, thioridazine and clozapine.Effects of microinjection of 6-hydroxydopamine (6-OHDA) into the striatum or nucleus accumbens on the cataleptogenic activity of these five neuroleptics were also investigated.

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“…The l-F antagonizes stereotypies induced by high doses of amphetamine and the hypermotility caused by lower doses of amphetamine (Bendotti et al 1980). However /-F does not share with haloperidol the property of decreasing the striatum acetylcholine content (Consolo et al 1975(Consolo et al , 1979 and does not antagonize stereotypies induced by apomorphine alone (Bendotti et al 1980).…”

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confidence: 91%

l-Fenfluramine and haloperidol in rats: a qEEG comparison

et al. 1989

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EEG effects of l-fenfluramine (l-F) (2.5, 5 and 10 mg/kg) and haloperidol (0.1, 0.25 and 0.5 mg/kg) were studied in 20 adult rats. The EEG signals of two prefrontal (A = +4, L = 2.5) and two sensorimotor (A = -4, L = 4) transcortical electrodes were analyzed in each rat during three 60-min periods, 1, 3 and 5 h after the intraperitoneal (IP) administration of the drugs. In the prefrontal cortex haloperidol induced a decreased power for the 1-3 Hz components and an increase in power for frequencies higher than 8 Hz, with a maximum around 13 Hz. These effects were already observed after 0.1 mg/kg. In this cortical area l-F administration was essentially associated with a decrease of power maximum for 3-8 Hz, an increased power for the 10-19 Hz band being present only after 10 mg/kg. In the sensorimotor cortex haloperidol appeared less potent than in the prefrontal site; a significant power increase for the frequencies higher than 8 Hz was only observed with 0.5 mg/kg. On the contrary, l-F appeared more effective in this area, its action being characterized by a decreased power from 2-8 Hz and a power increase already significant with 2.5 mg/kg for the frequencies higher than 10 Hz, with a maximum lying around 15 Hz. These results suggest that haloperidol induced cortical sedation (increased power) on the two recording sites. l-F also induced a net cortical sedation in sensorimotor cortex but up to 5 mg/kg acted in the opposite direction on the prefrontal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

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Decrease in rat striatal acetylcholine levels by some direct- and indirect-acting dopaminergic antagonists

Cited by 54 publications

References 24 publications

Action of apomorphine, bromocriptine and lergotrile onγ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

Action of apomorphine, bromocriptine and lergotrile onγ-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum

Effects of Bilateral Lesions in the Striatum or Nucleus Accumbens on the Cataleptogenic Activity of Neuroleptics in Rats

l-Fenfluramine and haloperidol in rats: a qEEG comparison

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