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Chronic cocaine enhances release of neuroprotective amino acid taurine: a microdialysis study

Elena Yablonski-Alter¹, Mervan Agovic², Eleonora Gashi², Theodore Lidsky³, Eitan Freedman¹ & Shailesh Banerjee⁴

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1. The City University of New York Medical School, Physiology and Pharmacology
2. Graduate School of the City University of New York, Biology and Neuroscience
3. New York State Institute for Basic Research in Developmental Disabilities
4. City University of New York Medical School

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Document Type:

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Date:

Received 22 September 2008 19:49 UTC; Posted 24 September 2008

Subjects:

Neuroscience, Pharmacology

Tags:

• Cocaine
• taurine
• neurotoxicity
• physiology
• Pharmacology
• neuroscience

Abstract:

Cocaine inhibits high-affinity neurotransmitter uptake at the presynaptic nerve terminals to increase synaptic levels of dopamine, norepinephrine and serotonin¹. This increase of synaptic dopamine may cause neurotoxicity^2,3. At least two different mechanisms have been proposed for the development of dopamine-related neurotoxicity: 1) dopamine produces a free radical that may induce cell toxicity^2,3 and 2) dopamine reduces glutamate transport at its presynaptic sites to increase synaptic levels of this amino acid⁴ and augments glutamate transmission by activating dopamine D1 receptors in different areas of the brain^5-7. Increase in glutamatergic transmission mediated by the activation on N-methyl dextro-aspartate (NMDA) receptors has been shown to cause excitotoxicity and neuro-degeneration⁸. Others and we have reported protection against different psychotropic drug-induced neurotoxicity that may be achieved by prior or simultaneous administration of various pharmacological agents. For example, repeated treatment of rats with haloperidol induced neuronal damage that is ameliorated by prior administration of either GM1 ganglioside⁹ or the endogenous amino acid, taurine¹⁰. Similarly, chronic gestational cocaine exposure causes neurotoxicity that could be prevented by co-administration of clozapine¹¹. To our knowledge, there is no information if chronic cocaine would enhance release of endogenous protective agents that may oppose the over activation of glutamatergic system. Here we show that repeated cocaine treatment increased synaptic levels of the neuroprotective amino acid taurine that opposes the excessive excitatory actions of the glutamatergic system in the rat brain. Thus, mammalian brain has an auto-protective mechanism to counter excitotoxicity and taurine or its synthetic derivative may be useful in the management and treatment of cocaine addiction and its neurotoxic effect.

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This document is licensed to the public under the Creative Commons Attribution 3.0 License

How to cite this document:

Yablonski-Alter, Elena, Agovic, Mervan, Gashi, Eleonora, Lidsky, Theodore, Freedman, Eitan, and Banerjee, Shailesh. Chronic cocaine enhances release of neuroprotective amino acid taurine: a microdialysis study. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2008.2319.1> (2008)

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