All of RAS components have been identified in the Central Nervous System. Angiotensin II, through its AT1 receptors activation, plays an active role as neuromodulator in the stress response and it is known its ability to modulate dopamine release and hippocampal activity in learning and memory processes.
It is known that acute exposure to psychostimulants, like amphetamine (AMPH) improves attention, meanwhile chronic exposure induces a disruption.
Our aim was to evaluate the involvement of brain RAS, through its AT1 receptors, on repeated amphetamine-induced behavioral and learning deficits.
Wistar male rats (250-300g), injected with AMPH (2,5 mg/kg, ip) for 5 days, pretreated with the AT1 receptor blocker (candesartan 3 mg/kg p.o.) were evaluated on the passive avoidance and holeboard test 1 week after the last exposure to the psychostimulant.
The results obtained indicated a facilitating effect in long term memory induced by the psychostimulant , and the AT1 blocker did not affected it. In respect to working memory, AMPH exposure impaired the performance in the holeboard test, this effect was prevented by the AT1 blocker. The same results were observed when the animal received an AMPH challenge before testing, in this case previous AT1 receptor blockade did not prevented it.
We conclude that AT1 receptors are involved in neurocognitive deficits induced by AMPH in working memory in basal conditions.
