Mechanisms of Acute Cocaine Toxicity

Kennon Heard*, 1, 2, Robert Palmer 1, Nancy R. Zahniser 3
1 Rocky Mountain Poison and Drug Center, Denver Health
2 Division of Emergency Medicine, University of Colorado Denver School of Medicine
3 Department of Pharmacology and Neuroscience Program, University of Colorado Denver School of Medicine, CO, USA

© 2008 Heard et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Rocky Mountain Poison and Drug Center, 777 Bannock St. MC 0180, Denver, CO 80204, USA; Tel: 303739-1475; Fax: 303 739-1264; E-mail:


Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporter, neurotransmitter receptor and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.

Keywords: Cocaine poisoning, dopamine receptor, serotonin receptor, sigma receptor, acetylcholine receptor.