Learned experiences are indispensable for adaptation and survival of every living organism. The generation of a memory trace is an active physiological process which implies association and organization of the new impressions with already stored ones. Therefore, memory is explained as activity-dependent synaptic plasticity, involving electrophysiological, biochemical and morphological changes in functional synapse.Throughout the different stages of information processing, emotion and memories interact to shape data encoding and retrieval. Dopamine plays a key role in the control of mood, fear and anxiety, and modulates the biochemical processes of memory. Hence, more plastic and appropriate responses can be achieved to variable external demands.Among drugs of abuse worldwide consumed, psychostimulants are known for their stimulant properties within the central nervous system. Monoaminergic neurotransmission elicited by amphetamine alters neuronal connectivity in several brain areas; thus, its pharmacological actions can be extended to learning and memory processes. Evidence indicates a complex scenario after psychostimulant administration where long-term memory can be either impaired or enhanced, according to the experimental conditions.Brain angiotensin II, by activation of its brain AT₁ receptors, plays an active role as neuromodulator in noradrenergic and dopaminergic transmission. AT₁ receptors activation positively regulates catecholamine synthesis and release, and their expression in brain areas is linked to noradrenaline and dopamine receptors. Angiotensin II AT₁ receptors are known to play a key role in acute responses as well as in the development of neuroadaptation induced by amphetamine. This evidence leads towards new modulatory pharmacotherapy approaches concerning psychostimulant-related alterations over cognitive processes.