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Nicotine recp mediated dopamine release and chronic nicotine

Institution: The Parkinson's Institute
Investigator(s): Xiomara Perez, Ph.D.
Award Cycle: 2006 (Cycle 15) Grant #: 15FT-0073 Award: $75,000
Subject Area: General Biomedical Science
Award Type: Postdoctoral Fellowship Awards
Abstracts

Initial Award Abstract
Parkinson’s disease is a debilitating disorder that affects over four million people over the age of 60 worldwide. The most common symptoms are resting tremor, muscular rigidity, bradykinesia (slowed movement) and postural instability. The cause of this neurodegenerative disorder is currently unknown. Strong evidence shows that smokers are less likely to develop Parkinson’s disease. These findings have sparked wide interest on finding the component of cigarette smoke responsible for the neuroprotective effect of smoking. Thus far, nicotine has become the main candidate reported to be responsible for protecting neurons from degeneration. Nicotine is known to stimulate the function of brain regions that are affected by Parkinson’s disease and some studies have shown that nicotine can protect nerve cells from being damaged. The long-term goal of the present proposal is to understand how nicotine may be executing its neuroprotection in Parkinson’s disease. Our preliminary data demonstrate that nicotine activates receptors in neurons responsible for motor control. The activation of these receptors leads to the release of chemicals in the brain that modulate the actions of these neurons. In this proposal we will investigate further how the activation of these receptors changes the kinetics of release in these neurons that control motor function. This will be done in control animals and also in animals with brain damage similar to that in Parkinson’s disease that have being treated chronically with nicotine. The results obtained in our studies will give us a better understanding of how nicotine changes the dynamics of receptor activation and release under physiological conditions and with disease. This information can then be used to develop therapeutics to prevent or stop the degeneration of neurons that leads to the symptoms of Parkinson’s disease.
Publications

Increased in dopamine release in primate putamen after nigrostriatal Damage
Periodical: Neuroscience Index Medicus:
Authors: Xiomara A. Perez ABS
Yr: 2006 Vol: Nbr: Abs: Pg:

Presynaptic dopaminergic compensation with moderate but not severe nigrostriatal damage in primate striatum
Periodical: Neuroscience Index Medicus:
Authors: Xiomara, Perez ABS
Yr: 2007 Vol: Nbr: Abs: Pg:

Chronic Nicotine Treatment Differentially Regulates Striatal a6a4B2B3* and a6B2B3* nAChr Expression and Function.
Periodical: Molecular Pharmacology Index Medicus:
Authors: Perez, XA; Bordia, TB; McIntosh, JM; Grady, SR; Quick, M. ART
Yr: 2008 Vol: Nbr: Abs: Pg:

Presynaptic Dopaminergic Compensation in Monkey Striatum After Moderate Nigostriatal Damage.
Periodical: Journal of Neurochemistry Index Medicus:
Authors: Perez, XA; Parameswaran, NP; Huang, LZ; O'Leary, KT; Quick, M. ART
Yr: 2008 Vol: 105 Nbr: 5 Abs: Pg: 1861-72

Increase in dopamine release in primate putamen after moderate but not severe nigrostriatal damage
Periodical: Society for Neuroscience Abstracts Index Medicus:
Authors: Perez, XA, NP Parameswaran, O'Leary, KT, Quik, M ABS
Yr: 0 Vol: Nbr: Abs: 100737 Pg:

Chronic nicotine treatment alters dopamine release in ventral but not dorsal striatum in non-human primates.
Periodical: Society for Neuroscience Abstracts Index Medicus:
Authors: Quik, M., Parameswaran, J.M., McIntosh, J.M., Perez, X.A. ABS
Yr: 0 Vol: Nbr: Abs: 104625 Pg: