Abstract
The acute administration of psychomotor stimulants, such as cocaine and amphetamine, produce behavioral activation in humans and increased locomotor activity in laboratory animals. These agents are also self-administered by various species by virtue of their reinforcing effects. It is generally accepted that these actions results, at least in part, from an increase in dopaminergic (DAergic) neurotransmission in the nucleus accumbens (NAc), a terminal projection region of dopamine (DA) neurons comprising the mesocorticolimbic system (1). Cocaine increases extracellular DA concentrations by binding to the DA transporter and inhibiting the uptake of DA from the synaptic cleft, whereas amphetamine causes a reversal of the DA transporter and increases DA release (2,3).
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Shippenberg, T.S., Chefer, V.I. (2003). Opioid Modulation of Psychomotor Stimulant Effects. In: Maldonado, R. (eds) Molecular Biology of Drug Addiction. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-343-9_7
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