Cocaine, UTC for healthcare professionals
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Among its multiple mechanisms of pharmacological action, cocaine blocks the reuptake of noradrenaline and serotonin (Feldman, 1997) and indirectly produces sympathomimetic effects (increased blood pressure, tachycardia, pupillary dilation, sweating, vasoconstriction, tremor, etc.) because it does not act directly on adrenergic or dopaminergic receptors. Regarding the development of dependence, it blocks the dopamine transporter protein, so that neurotransmitter accumulates in the synapsis and magnifies the pleasant and reinforcing effects of consumption (NIDA, 2016).
Chronic consumption enables brain neuroadaptation as a compensatory response to the artificial over-stimulation produced by the drug. Modern neuroimaging techniques corroborate this adaptation, demonstrating that the brains of people dependent on cocaine show considerably fewer dopaminergic receptors, specifically subtype D2 (Volkow, 2004). These long-term effects may explain the symptoms of depressed mood and lack of pleasure, experienced during the withdrawal syndrome.
- Feldman, R., Meyer, J., & Quenzer, L. (1997). Principles of Neuropsychopharmacology. Massachusetts: Sinauer Associates, Inc. Publishers.
- NIDA. (2016, May 6). Cocaine. Retrieved from https://www.drugabuse.gov/publications/research-reports/cocaine
- Volkow, N. Fowler, J., & Wang, G. (2004). The addicted human brain viewed in the light of imaging studies: brain circuits and treatment strategies. Neuropharmacology, 47, 3 – 13.
UTC for healthcare professionals
- Neurobiology of Addiction: https://www.issup.net/node/7342
- Classification of Drugs: https://www.issup.net/node/7521
Consequences of cocaine use