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Partial amnesia was induced in rats by electroconvulsive shock (ECS) immediately after passive avoidance learning. This partial amnesia could be prevented by administering porcine brain natriuretic peptide-32 (pBNP-32) into the lateral brain ventricle. The effects of pretreatment with different receptor blockers (haloperidol, atropine, phenoxybenzamine, propranolol, naloxone, bicuculline and methysergide) on the pBNP-32-induced antiamnesia were investigated. In the doses selected, the blockers had no influence on the ECS-induced amnesia. Haloperidol, atropine, phenoxybenzamine and propranolol blocked the antiamnesic action of the peptide, while naloxone, bicuculline and methysergide were ineffective. These results suggest that pBNP-32 may influence learning processes and that the antiamnesic action of this peptide is mediated by dopaminergic, cholinergic α- and β-adrenergic mediator systems.

In previous experiments, it was observed that rat atrial natriuretic peptide-(1–28) (ANP-(1–28)) participated in fear-induced learning and memory processes via dopaminergic and cholinergic mediation. Since cage-climbinh behavior is described as a simple test for studying dopaminergic activity in the central nervous system, a systematic study was carried out with ANP-(1–28) in order to confirm or to exclude the possible involvement of dopamine in the ANP-induced action in the brain. The present study demonstrates that ANP-(1–28) facilitated cage-climbing behavior in mice in a dose-dependent manner. When combined with apomorphine, the peptide potentiated the effect of the dopamine agonist. The effect of ANP-(1–28) in combination with apomorphine could be antagonized by a selected dose of haloperidol. These data suggest that ANP might be regarded as a dopamine agonist-modulating agent and that a dopaminergic mechanism is a possible mode of action of ANP in the fear-induced learning studied earlier.