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Cocaine crosses the blood-brain barrier via a proton-coupled organic cation antiporter[18][19] and (to a much lesser extent) via passive diffusion.[20] Cocaine acts as an indirect sympathomimetic by blocking the dopamine transporter,[21] inhibiting reuptake of dopamine from the synaptic cleft into the pre-synaptic axon terminal; the higher dopamine levels in the synaptic cleft increase dopamine receptor activation in the post-synaptic neuron,[22][23] which drives the effects of euphoria and arousal.[24] Cocaine also blocks the serotonin transporter and norepinephrine transporter, inhibiting reuptake of serotonin and norepinephrine from the synaptic cleft into the pre-synaptic axon terminal and increasing activation of serotonin receptors and norepinephrine receptors in the post-synaptic neuron, contributing to the modulation of consciousness, emotions, and movements that characterize cocaine exposure.[25] Cocaine is addictive due to its effect on the reward pathway in the brain.[16] A single dose of cocaine induces tolerance to the drug's effects. After a short period of use, dependence is likely.[16] Abstention from cocaine after chronic use results in drug withdrawal, with symptoms that may include depression, decreased libido, decreased ability to feel pleasure and subjective fatigue.[16] Cocaine's use increases the overall risk of death and particularly the risk of trauma, and infectious diseases, such as blood infections and AIDS. It also increases risk of stroke, heart attack, cardiac arrhythmia, lung injury (when smoked), and sudden cardiac death.[16][26] Illicitly sold cocaine is commonly adulterated with local anesthetics, levamisole, cornstarch, quinine, or sugar, which can result in additional toxicity.[27] The Global Burden of Disease study found that cocaine use caused around 7300 deaths in 2007.[28]