June, 2010Researchers at The University of Texas at San Antonio 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.
Typically, dopaminergic neurons fire fast bursts of electrical activity. But how do they manage to fire such fast bursts? Scientists widely agree a protein called the NMDA receptor, in the neuron’s outer membrane, has something to do with it.
UTSA Assistant Professor Carlos Paladini and UTSA 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. Through a series of studies, the researchers observed that the NMDA receptor is highly sensitive to voltages. When outer membrane’s voltage is more positive, the NMDA receptor channel opens and leads to a single spike of electrical activity. When 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.
The result? Because the dopaminergic neuron’s voltages quickly alternate between positive and negative, NMDA receptors will also quickly alternate between open and closed states. That is, voltage cues cause the NMDA receptors to rapidly oscillate 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.
Because dopaminergic neurons are the neurons that die during Parkinson’s disease and they are also the neurons that are affected when a drug user takes psychostimulants such as cocaine and amphetamine, the research has profound implications for public health.
“For some reason, dopaminergic neurons are vulnerable in Parkinson’s Disease,” says Paladini. “This study helps us better understand the physiology underlying their vulnerability.”
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