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WesternU Team Advances Understanding of Mechanisms of Learning and Neural Degeneration
Date:1/7/2014

in LTP, and in learning and memory.

“That’s where we got the big breakthrough. When we put this calpain inhibitor after the train to induce LTP, we found that it enhanced the magnitude of long-term potentiation,” Baudry said. “This only takes place during a short period of time after a train of high-frequency stimulation. If we give the inhibitor one hour after, it has no effect. Between 0 and 1 hour, activation of m-calpain restricts the extent of potentiation. That’s why we call it a molecular brake.

“People have known for a very long time that if you want to learn, it’s better to space the learning trials,” he added. “Repetition facilitates learning, but it’s better to space the repetition rather than cram it into a short period of time. We think that this molecular brake is responsible for this effect.”

The second paper, “Distinct Roles for mu-Calpain and m-Calpain in Synaptic NMDAR-Mediated Neuroprotection and Extrasynaptic NMDAR-Mediated Neurodegeneration,” by Yubin Wang, Victor Briz, Athar Chishti, Xiaoning Bi and Michel Baudry, published in The Journal of Neuroscience as a feature article, looks at the roles of the same two calpain isoforms, (mu- and m-) in the consequences of prolonged activation of NMDA receptors, which are glutamate receptors that are critical for learning. Click here to view the article: http://www.jneurosci.org/content/33/48/18880.

A brief activation of the NMDA receptor will provide a brief influx of calcium, which will produce long-term potentiation. But if you overactivate the receptor, you produce a massive influx of calcium, which can then lead to neural degeneration, Baudry said.

There are two types of NMDA receptors – synaptic receptors and extrasynaptic NMDA receptors, which are located on the surface of neurons but not at synaptic sites.

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