Now the famous saying practice makes perfect has received some scientific backing, for neuroscientists from Carnegie Mellon University and the Max Planck Institute have identified the novel mechanism behind long-term learning.
Washington, Jan 4 : Now the famous saying 'practice makes perfect' has received some scientific backing, for neuroscientists from Carnegie Mellon University and the Max Planck Institute have identified the novel mechanism behind long-term learning.
According to the research team, the mechanism explains how brain synapses strengthen in response to new experiences.
Earlier study by Carnegie Mellon researcher and lead author of the study Alison Barth has shown that there is a link between synaptic plasticity, or changes, and learning and memory. However, not much was known about the mechanisms that trigger learning that occurs over longer timeframes, with continuing training or practice.
Now, the team has shown that N-methyl-D-aspartate (NMDA) receptors are required to initiate synaptic plasticity in this mechanism, a fact that holds true in many areas of the brain.
Barth and colleagues discovered that the NMDA receptors experience a sort of Jekyll-and-Hyde transition after an initial phase of learning. Instead of helping synapses get stronger, they actually begin to weaken the synapses and impair further learning.
"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.
Barth opted 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 researchers then 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 brain's cortex, making it easy to monitor activity and changes. Limiting the mouse's 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. Establishing the relationship between NMDA and mGlu receptors will allow us to better understand how we learn and perhaps may help us better understand diseases where learning and memory is lost, as in Alzheimer's disease," said Barth.
The findings are published in the Jan. 4 issue of Science.
ANI