Dissociative effects of apomorphine infusions into the medial prefrontal cortex of rats on latent inhibition, prepulse inhibition and amphetamine-induced locomotion.

Impaired ability to "gate out" sensory and cognitive information is considered to be a central feature of schizophrenia and is manifested, among others, in disrupted prepulse inhibition and latent inhibition. The present study investigated, in rats, the effects of increasing dopamine receptor activation within the medial prefrontal cortex by local administration of the dopamine receptor agonist apomorphine (9 microg/side) on prepulse inhibition and latent inhibition, as well as on spontaneous and amphetamine-induced activity. Apomorphine infusions decreased spontaneous locomotor activity and blocked amphetamine-induced increase in locomotor activity in the open field, which is in line with the suggestion that dopamine receptor activation in the medial prefrontal cortex inhibits mesolimbic dopamine activity. However, apomorphine infusions induced a disruption of prepulse inhibition, an effect associated with increased dopaminergic activity in the nucleus accumbens, and left the latent inhibition effect intact. While these results support previous evidence that the medial prefrontal cortex is a component of the neural circuitry mediating prepulse inhibition but plays no role in latent inhibition, they show that dopamine receptor activation in the medial prefrontal cortex of the rat produces behavioural outcomes that cannot be explained by postulating a simple reciprocal relationship between the mesocortical and mesolimbic dopamine systems.