Northwestern Medicine scientists have discovered a new form of cell learning in the striatum, a region of the brain involved in motor control as well as the symptoms of Parkinson’s disease and schizophrenia.
Specifically, the scientists found that the neurotransmitter nitric oxide decreases the strength of communication between some neurons. This is a form of synaptic plasticity, a process in which neuronal pathways adapt as they learn from new stimuli. The results of the study were published in Cell Reports.
“Nitric oxide is released from a small, local population of striatal cells called interneurons,” said co-first author Alexandria Melendez, a graduate student in the Medical Scientist Training Program (MSTP). “For years, the importance of this particular population has seemed nominal at best. Our study demonstrates that this is not the case.”
Among its many tasks, the striatum is responsible for controlling movement and mediating the reward system. When processes like synaptic plasticity malfunction in this brain region, it can affect those tasks and lead to disease.
“By building a better framework of how the striatum functions in a healthy brain, we can begin to better understand what is going wrong in disease and use these observations and hypotheses to come up with treatments that the field is in great need of,” Melendez said.
Working with senior author D. James Surmeier, PhD, chair and Nathan Smith Davis Professor of Physiology, Melendez and co-author Asami Tanimura, PhD, physiologically induced nitric oxide to release from interneurons using optogenetics, a biological technique that uses light to control genetically-modified neurons. The research team witnessed a decrease in cell communication that was similar to what that they saw through pharmacological manipulations.
In continuing research, Melendez is exploring what neurotransmitters modulate nitric oxide releasing interneurons and how these cells change in Parkinson’s disease.
This study was supported by National Institutes of Health (NIH) grant NS34696, the JPB Foundation, the Cure Huntington’s Disease Initiative, National Science Foundation grant 610-5108000-60032448 and fellowships from the NIH and the Japan Society for the Promotion of Science Postdoctoral Fellow for Research Abroad.
