Neuroleptic antagonism of the motor inhibitory effects of apomorphine within the nucleus accumbens: Drug interaction at presynaptic receptors?

The hypomotility elicited by small doses of apomorphine seems exclusively mediated by dopaminergic systems in the nucleus accumbens

“…Injections of dopamine, L-DOPA, amphetamine or apomorphine into the nucleus accumbens stimulate locomotor activity in laboratory animals (Andrn and Jackson, 1975;Costall et al, 1976;1980;Pijnenburg et al, 1976).…”

Neonatal hippocampal lesion model of schizophrenia in rats: Sex differences and persistence of effects into maturity

“…Almost all current animal models of schizophrenia depend on pharmacological rather than neurodevelopmental perturbations of the brain and many of these models are predicated on activation of the dopamine system [Arnt et al, 1994;Costall et al, 1980;Sorensen et al, 1993]. Accordingly, these models focus on examining dopamine antagonism and, in particular, the antagonism of the dopamine D 2 receptor, rather than examining an "antipsychotic effect" per se.…”

Effects of low, autoreceptor selective doses of dopamine agonists on the discriminative cue and locomotor hyperactivity produced by d-amphetamine

“…The present study has demonstrated that other DA agonists, such as quinpirole and (+)-3-PPP, can block this behavioural stimulation when they are administered in doses thought to selectively activate DA autoreceptors. The inhibitory effects of quinpirole and (+)-3-PPP are likely to be at least partially mediated by DA receptors in the nucleus accumbens, since direct injections of low concentrations of apomorphine into this brain region reduce the hyperactivity produced by d-amphetamine in a DA antagonist-reversible manner (Costall et al, 1980). It seems reasonable to suggest that these sites are DA autoreceptors located on DA presynaptic terminals, stimulation of which would lead to a reduction in d-amphetamine-induced release of the transmitter.…”

“…In laboratory animals, selective activation of DA autoreceptors results in sedation and inhibition of spontaneous locomotor activity (Strombom, 1975;Hjorth et al, 1981;Sffthle and Ungerstedt, 1987). The locomotor hyperactivity produced by damphetamine can also be reduced by low doses of the DA agonist apomorphine, administered either systemically (Creese etal., 1982;Strombom and Leidman, 1982;Kuczenski etal., 1990) or directly into the nucleus accumbens (Costall et al, 1980). These findings suggest that selective stimulation of DA autoreceptors may be effective in the management of disorders associated with a hyperactivity of brain DA systems, such as schizophrenia and tardive dyskinesia.…”