"It first appeared odd to us that an immature inhibitory synapse would want to release an excitatory neurotransmitter. After all, this contradicts the most basic principles that have defined the field of neuroscience. But when we also found that this glutamate activates NMDA receptors at the most critical stage of brain development and organization, we realized that this could explain a number of fundamental questions," explained Karl Kandler, Ph.D., associate professor of neurobiology at the University of Pittsburgh School of Medicine, and the study's senior author.
"These findings shed new light on how inhibitory synapses evolve and are assembled into functional circuits in the developing brain," he added.
Many brain disorders, like epilepsy, schizophrenia and depression, involve deficits that prevent normal inhibition of cells. Dr. Kandler's research could eventually provide insight into the biological cause of these disorders and help to identify novel approaches for prevention and treatment. Further study could have particular implications for dyslexia and tinnitus ?often referred to as ringing in the ears ?which can be caused by abnormal inhibitory signaling within the auditory system, a region of the brain that is the focus of Dr. Kandler's research.
Before there can be practical clinical applications several questions need to be answered, including how GABA, glycine and glutamate synapses cooperate to activate NMDA receptors. In the traditional sense, when inhibitory synapses are mature, they would never release glutamate, nor would they be able to depolarize a cell, both of which are required for NMDA receptor
Source:University of Pittsburgh Medical Center