The effects of drugs that alter neurotransmission of dopamine, norepinephrine, and serotonin have been studied extensively in relation to BSR. Neurochemical studies have shown that BSR results in the release of dopamine within the nucleus accumbens. This effect is generally potentiated following administration of drugs that themselves increase the amount of extracellular dopamine in the nucleus accumbens, such as cocaine, which inhibits re-uptake of dopamine to the intracellular space by blocking its transporter. Conversely, these levels are decreased and the rewarding properties of BSR are blocked following administration of drugs that antagonize dopamine receptors or reduce the amount of extracellular dopamine, by promoting either degradation or re-uptake of the neurotransmitter. While dopamine is generally considered to be the main neurotransmitter implicated in the reward system, it is often not the only neurotransmitter affected by addictive, monoaminergic drugs. Importantly, the circuitry involved in BSR is multi-synaptic and not exclusively dopaminergic. This introduces potential for modulation by other neurotransmitter systems at different stages in the transmission of the reward signal.