[Disruption of latent inhibition in adult rats after prepubertal dopamine terminals lesions in the ventral hippocampus].

Wistar rats were submitted to bilateral ventral hippocampal injection of 6-hydroxydopamine on 32nd day after birth. Latent inhibition was measured in passive or active avoidance tasks when the rats received 20 and 100 pre-exposures of conditioned stimulus. Prepubertal and adult lesioned rats showed a deficit in the latent inhibition but not in the capacity to avoidance learning in presence of the conditioned stimulus novelty. Possible mechanism of the involvement of hippocampal dopaminergic terminals in attention inhibition to irrelevant information is considered.

[Involvement of dopamine receptors of different types in formation of latent inhibition of passive avoidance reaction in Wistar rats].

The effect of the intraperitoneal injection of dopaminergic agents on normal and weak latent inhibition of step-through passive avoidance task was studied in rats. Normal latent inhibition was caused by 20-fold preexposure (four times daily) of environmental conditional stimulus before training. For modeling of the weak latent inhibition 10-fold preexposure was used. Effects of D2 agonist quinpirole (1 mg/kg) and selective D1 agonist SKF 38393 (1 mg/kg) injected individually and in combination with haloperidol (0.5 mg/kg) were tested. Quinpirole caused a significant potentiation of the normal latent inhibition (20-fold preexposures) but did not affect the weak latent inhibition. Haloperidol reinforced the weak latent inhibition but reduced the normal latent inhibition. The agent SKF 38393 was not able to affect the latent inhibition independently of the preexposure number. Injected in combination with haloperidol, SKF 38393 prevented the normal latent inhibition from being impaired by haloperidol. These findings suggest that D1 receptors do not appear to participate in the modulation of the latent inhibition as an independent substrate, but D1 receptors are essential for the full manifestation of the D2-mediated modulation of the latent inhibition.