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UTSA brain research offers lead in treatment of Parkinson's disease
(May 14, 2010)--Researchers at the UTSA Neurosciences Institute are one step closer to understanding the physiology of dopaminergic neurons, the neurons in the brain that generally produce dopamine but die during Parkinson's disease.
Because dopaminergic neurons are the neurons that die during Parkinson's disease, and they also are the neurons affected when a drug user takes psycho-stimulants such as cocaine and amphetamine, the research has profound implications for public health.
Typically, dopaminergic neurons fire fast bursts of electrical activity. Scientists widely agree a protein called the NMDA receptor in the neuron's outer membrane has something to do with the ability to fire such fast bursts.
UTSA Assistant Professor Carlos Paladini and Professor Charles Wilson in the Department of Biology set out to learn how NMDA receptors cause bursts of firing in the brain's dopaminergic neurons. In a series of studies, the researchers observed that the NMDA receptor is highly sensitive to voltages. When the outer membrane's voltage is more positive, the NMDA receptor channel opens and leads to a single spike of electrical activity. When the outer membrane's voltage is more negative, the NMDA receptor channel closes and allows the neuron to recover from the previous spike of electrical activity.
Because the dopaminergic neuron's voltages quickly alternate between positive and negative, the result is NMDA receptors also quickly alternate between open and closed states. Voltage cues cause the NMDA receptors to oscillate rapidly several times between a spike of electrical activity one moment and silence the next, allowing dopaminergic neurons to fire a rapid burst of spikes: one spike with each NMDA receptor oscillation.
"For some reason, dopaminergic neurons are vulnerable in Parkinson's disease," said Paladini. "This study helps us better understand the physiology underlying their vulnerability."