We know intuitively that the more we practice something, the better we get, so there had to be something that happened after the NMDA receptors switched function which helped synapses to continue to strengthen, said Barth, an assistant professor of biological sciences at the universitys Mellon College of Science.
Barth chose to look at the cortex, an area of the brain responsible for a slower form of learning that can improve with additional training, or experience. She notes that this brain area may use very different molecular mechanisms than other forms of short-term, episodic memory like those that may occur in the hippocampus.
In a series of experiments the researchers blocked different receptors, including NMDA, to see the receptors effect on long-term neural stimulation. They found that while the NMDA receptor is required to begin neural strengthening, a second neurotransmitter receptor the metabotropic glutamate (mGlu) receptor comes into play after this first phase of cellular learning. Using an NMDA antagonist to block NMDA receptors after the initiation of plasticity resulted in enhanced synaptic strengthening, while blocking mGlu receptors caused strengthening to stop.
The Carnegie Mellon researchers tracked the changes in the neurons by using a transgenic mouse model that Barth created. In the model, a mild sensory imbalance is created by allowing the mouse to sense its surrounding through only one whisker. Whiskers are useful in studying sensory plasticity because, like human fingers, each whisker is linked to its own unique area of the brains cortex, making it easy to monitor activity and changes. Limiting the mouses ability to sense its surroundings through only one whisker causes a sensory imbalance leading to increased plasticity in the cortex.
The neural mechanisms of learning and memory have been poorly understood, said Barth. Establishing the relationship between NMDA and mGlu rece
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Carnegie Mellon University