ArticleNeuroscience2007
Cocaine exposure in vitro induces apoptosis in fetal locus coeruleus neurons by altering the Bax/Bcl-2 ratio and through caspase-3 apoptotic signaling.
Article in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Dimethyltryptamine and harmine, components of ayahuasca, prevented cocaine-induced apoptosis in SH-SY5Y human neuroblastoma cells.Archives of toxicology · 2026Article
- Review
- Anhydroecgonine methyl ester, a cocaine pyrolysis product, contributes to cocaine-induced rat primary hippocampal neuronal death in a synergistic and time-dependent manner.Archives of toxicology · 2021Article
- Noradrenergic correlates of chronic cocaine craving: neuromelanin and functional brain imaging.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- MiR-9, miR-153 and miR-124 are down-regulated by acute exposure to cocaine in a dopaminergic cell model and may contribute to cocaine dependence.Translational psychiatry · 2018Article
- A Comprehensive View of the Neurotoxicity Mechanisms of Cocaine and Ethanol.Neurotoxicity research · 2015Review
- Cocaine Causes Apoptotic Death in Rat Mesencephalon and Striatum Primary Cultures.BioMed research international · 2015Article
- Influence of the dopaminergic system, CREB, and transcription factor-κB on cocaine neurotoxicity.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2013Article
- 17β-estradiol impedes Bax-involved mitochondrial apoptosis of retinal nerve cells induced by oxidative damage via the phosphatidylinositol 3-kinase/Akt signal pathway.Journal of molecular neuroscience : MN · 2013Article
- Cyclic AMP response element modulator-1 (CREM-1) involves in neuronal apoptosis after traumatic brain injury.Journal of molecular neuroscience : MN · 2012Article
- Prenatal cocaine exposure alters progenitor cell markers in the subventricular zone of the adult rat brain.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2012Article
- Cocaine modulates the expression of opioid receptors and miR-let-7d in zebrafish embryos.PloS one · 2012Article
- Chamaejasmine induces apoptosis in human lung adenocarcinoma A549 cells through a Ros-mediated mitochondrial pathway.Molecules (Basel, Switzerland) · 2011Article
- Ginsenoside Rg3 inhibit hepatocellular carcinoma growth via intrinsic apoptotic pathway.World journal of gastroenterology · 2011Article
- Linking cocaine to endoplasmic reticulum in striatal neurons: role of glutamate receptors.Basal ganglia · 2011Article
- Prenatal IV Cocaine: Alterations in Auditory Information Processing.Frontiers in psychiatry · 2011Article
- Cocaine induces cell death and activates the transcription nuclear factor kappa-B in PC12 cells.Molecular brain · 2009Article
- Neurotoxic profiles of HIV, psychostimulant drugs of abuse, and their concerted effect on the brain: current status of dopamine system vulnerability in NeuroAIDS.Neuroscience and biobehavioral reviews · 2008Review
- Substantia nigra MR imaging signal changes and cardiomyopathy following prenatal exposure to cocaine and heroin.AJNR. American journal of neuroradiology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Cocaine inhibits survival and growth of rat locus coeruleus (LC) neurons, which may mediate alterations in attention, following in utero exposure to cocaine. These effects are most severe in early gestation during peak neuritogenesis. Prenatal cocaine exposure may specifically decrease LC survival through an apoptotic pathway involving caspases. Dissociated fetal LC neurons or substantia nigra (SN) neurons (control) were exposed in vitro to a pharmacologically active dose of cocaine hydrochloride (500 ng/ml) and assayed for apoptosis using terminal deoxynucleotidyl transferase mediated DNA nick end labeling and Hoechst methodologies. Cocaine exposure decreased survival and induced apoptosis in LC neurons, with no changes in survival of SN neurons. Activation of apoptotic signal transduction proteins was determined using enzyme assays and immunoblotting at 30 min, 1 h, 4 h and 24 h. In LC neurons, Bax levels were induced at 30 min and 1 h, following cocaine treatment, and Bcl-2 levels remained unchanged at all time points, altering the Bax/Bcl-2 ratio. The ratio was reversed for SN neurons (elevated Bcl-2 levels and transient reduction of Bax levels). Further, cocaine exposure significantly increased caspase-9 and caspase-3 activities at all time points, without changes in caspase-8 activity in LC neurons. In addition, cleavage of caspase-3 target proteins, alpha-fodrin and poly (ADP-ribose) polymerase (PARP) were observed following cocaine treatment. In contrast, SN neurons showed either significant reductions, or no significant changes, in caspase-3, -8 or -9 activities or caspase-3 target proteins, alpha-fodrin and PARP. Thus, cocaine exposure in vitro may preferentially induce apoptosis in fetal LC neurons putatively regulated by Bax, via activation of caspases and their downstream target proteins.
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