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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 alpha- and beta-adrenergic mediator systems.

The effects of two doses of rat atrial natriuretic peptide (TANP-1-28), 200 and 500 ng, on 6-day acquisition and extinction of food-reinforced conditional learning (conditional stimulus: light) were studied in rats following administration into the lateral cerebroventricle. With the higher dose, there was a tendency for facilitated acquisition and significantly delayed extinction of the positively reinforced learning task. In order to clarify whether the effect of the peptide is obtained through the involvement of neurotransmitters, the experimental animals were pretreated with different receptor blockers in selected doses that did not influence the behavioral test. Haloperidol, atropine, phenoxybenzamine, and propranolol blocked the action of ANP on extinction of the food-reinforced conditioning, whereas naloxone, bicuculline, and methysergide were ineffective. The results suggest that ANP might be considered a modulating agent in a positively reinforced conditional learning task, and that its action might involve dopaminergic, cholinergic, and alpha- and beta-adrenergic mechanisms.

Three doses of porcine brain natriuretic peptide (pBNP-32) were tested in regards to the extinction of active avoidance behavior following injection into the lateral brain ventricle in rats. This peptide delayed the extinction of the active avoidance reflex in a dose-dependent manner. To clarify the involvement of transmitters in the action of the peptide, the animals were pretreated with different receptor blockers in doses that did not affect the behavior of the animals in this learning paradigm. Dopaminergic, cholinergic, and alpha- and beta-adrenergic blockers effectively blocked the delaying action of pBNP-32, whereas GABAergic, serotoninergic, and opiateergic blockers were ineffective. The data suggest that the delaying action of pBNP-32 on the extinction of active avoidance behavior is mediated via dopaminergic and alpha- and beta-adrenergic neuromediations.

The effect of rat atrial natriuretic peptide (ANP1-28) on the pargyline-DOPA potentiation test was studied following its administration into the lateral brain ventricle in mice. Thirty minutes after pargyline pretreatment, three doses of ANP (200, 500, or 1,000 ng/mouse) were administered simultaneously with DOPA and animals were then observed for 2 h. ANP in doses of 500 and 1,000 ng markedly enhanced the effect of DOPA. The maximum intensity of the effect was registered 30-45 min following administration of the peptide. The data suggest that ANP might be regarded as a dopaminergic-modulating agent in the CNS.

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-climbing behavior is described as a simple test for studying dopaminergic activity in the central nervous system, a systemic 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 demonstrate 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.

The effects of rat atrial natriuretic peptide (ANP 1-28) on passive avoidance behaviour were tested following its administration into the lateral brain ventricle in rats. Different doses of ANP 1-28 were administered immediately after the learning trial of passive avoidance behaviour and the effects on the consolidation of learning were tested 24 h later. ANP 1-28, in doses in the range 50-2000 ng/rat, caused a dose-dependent increase in passive avoidance latency. Selected doses (100, 200 and 500 ng/animal) were given 30 min before the learning trial. These doses lengthened the passive avoidance latency in a dose-dependent manner. When the peptide was given 30 min before the retention trial, there was no significant alteration in passive avoidance response. The data suggest that ANP 1-28 is able to facilitate the learning and consolidation of fear-motivated passive avoidance behaviour.