Gene/Protein Disease Symptom Drug Enzyme Compound
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Toxic effects of cocaine on the heart muscle have been known for many years. Cardiovascular complications related to cocaine abuse include myocardial ischemia and infarction, inflammation, and disease of the heart muscle, rhythm disturbances, and sudden cardiac death. Cocaine toxicity-related cardiac morbidity and mortality are often due to several interacting mechanisms. Cocaine also has a potent pharmacological effect, indirectly stimulating the sympathetic nervous system, and it has a direct toxic effect on the heart. Although apoptosis (also called programmed cell death) has been shown to play an important role in the pathogenesis of several diseases in the heart, including heart failure and ischemic myocardial infarction, the role of apoptosis in the toxic effect of cocaine on the heart has not been explored. Recent studies indicated that cocaine causes apoptotic cell death in both adult and fetal heart muscles. Increased oxidative stress and reactive oxygen species, and the subsequent activation of a "stress responsive" enzyme (p38-mitogen-activated protein kinase) in the heart may play an important role in cocaine-induced apoptosis in the heart muscle. These findings suggest a new way to understand the cardiotoxic effects of cocaine, and may have potential clinical implications in the better management of cocaine-induced heart diseases. Anat Rec (New Anat): 257:208-216, 1999.
Anat Rec 1999 12 15
PMID:Cocaine and apoptosis in myocardial cells. 1062 Jul 50

Previous studies have shown significant changes in dopamine and opioid receptors in the basal ganglia following administration of cocaine. Cocaine administration results in a significant increase in the number of opioid receptors in dopamine-enriched brain regions. The aim of this study was to determine if dopamine D2 receptors (D2r) and micro-opioid receptors (microOr) are localized to the same neurons in the dorsolateral striatum. Immunoperoxidase and immunogold-silver labeling combined with electron microscopy was used to examine the ultrastructural localization of both receptors in the dorsolateral striatum. Approximately half of the microOr-labeled somatodendritic processes showed immunolabeling for the D2r. Similarly, about half of the D2r-labeled dendrites and cell bodies showed immunolabeling for the microOr. In conclusion, our results indicate that individual neurons in the rat dorsolateral striatum may be directly modulated by both dopaminergic and opioid ligands. These data also suggest that the molecular mechanism responsible for the up-regulation of microOrs in the caudate and putamen following cocaine exposure may depend, in part, on the co-existence of D2rs and micro-Ors in these cells.
Anat Rec A Discov Mol Cell Evol Biol 2004 Jul
PMID:Ultrastructural evidence for co-localization of dopamine D2 and micro-opioid receptors in the rat dorsolateral striatum. 1522