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• W1994425512 abstract "Intra-accumbens d-amphetamine caused a dose-dependent hyperactivity which was shown to involve the release of newly synthesized dopamine. The amphetamine response was antagonised by apomorphine in a narrow dose range. This antagonistic effect of apomorphine was specifically inhibited by the neuroleptic agents pimozide and haloperidol in doses too low to inhibit the amphetamine response per se. Also, apomorphine exerted its antagonistic effect only when administered directly into the nucleus accumbens, not when injected into the caudateputamen or tuberculum olfactorium. Further, doses of intra-accumbens apomorphine which antagonised the amphetamine response reduced the homovanillic acid content of the nucleus accumbens but not that of the caudateputamen or tuberculum olfactorium. The apomorphine induced change in accumbens homovanillic acid was antagonised by haloperidol at doses effective in the behavioural experiments. Finally, the ability of apomorphine to antagonise amphetamine hyperactivity was abolished following the intra-accumbens injection of 6-OHDA (the amphetamine response being maintained after lesion) which specifically destroyed dopamine nerve terminals in the nucleus accumbens. This data is forwarded to support a general conclusion that intra-accumbens apomorphine antagonises the hyperactivity induced by intra-accumbens amphetamine by an action at neuroleptic sensitive sites within the nucleus accumbens and which may be located on nerve terminals, i.e. presynaptic receptors. The ability of neuroleptic agents to antagonise at postsynaptic dopamine receptors (antagonise the amphetamine response per se) was compared with an ability to reverse the apomorphine antagonism of the amphetamine response at a hypothesised ‘presynaptic receptor’. A differential dose could not be determined for clozapine of thioridazine. For pimozide and haloperidol the ratio of pre- to postsynaptic activity was small, whilst (−)-sulpiride was 5 fold more effective to inhibit pre- than postsynaptic receptors. This data provides support for the hypothesis that there may exist more than one neuroleptic mechanism in the nucleus accumbens which contribute to an overall control of motor function via the mesolimbic system." @default.
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• W1994425512 date "1980-05-01" @default.
• W1994425512 modified "2023-10-18" @default.
• W1994425512 title "Neuroleptic antagonism of the motor inhibitory effects of apomorphine within the nucleus accumbens: Drug interaction at presynaptic receptors?" @default.
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• W1994425512 doi "https://doi.org/10.1016/0014-2999(80)90265-4" @default.
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