Research sheds light on memory by erasing it

May 08, 2007

For years, scientists have studied the molecular basis of memory storage, trying to find the molecules that store memory, just as DNA stores genetic memory. In an important study published this week in the Journal of Neuroscience, Brandeis University researchers report for the first time that memory storage can be induced and then biochemically erased in slices of rat hippocampus by manipulating a so-called "memory molecule," a protein kinase known as CaMKII.

"The core problem in memory research has been understanding what the storage molecule actually is. Identifying this molecule is essential to understanding memory itself as well as any disease of memory, " explained lead author John Lisman. "With this study, we have confirmed CaMKII as a memory molecule."

The research involved electrically stimulating neuronal synapses to strengthen them, a process known as long-term potentiation (LTP). This process has served as a model system for studying memory. CaMKII has been a leading candidate as a memory molecule because it is persistently activated after LTP induction and can enhance synaptic transmission, properties that are necessary for a memory molecule.

Like a computer whose electronics change with the addition of new information, molecular activity in the hippocampus, where memory is stored in the brain, changes as memory is being stored. In this study, Lisman and his colleagues showed that they could saturate the memory stores. However, when CaMKII was chemically attacked and previous memory erased, it then became possible to insert new memories in the synapses.

Alzheimer's and other diseases in which memory loss plays a major role will benefit from this new understanding. Of particular importance may be conditions like epilepsy, which involves synapses that have become overly strengthened. The new research shows how synapses can be weakened by attacking memory molecules.

Lisman's lab plans further research to better understand what happens to the CaMKII after it is attacked. By using fluorescent forms of CaMKII, it will be possible to determine whether the kinase leaves the synapse after inhibitor is applied. This provides a way to directly visualize the forgetting process and complements previous work done in Lisman's laboratory showing that when LTP is induced (as during learning), CaMKII moves into the synapse.

Source: Brandeis University

Explore further: New compounds protect nervous system from the structural damage of MS

add to favorites email to friend print save as pdf

Related Stories

Recommended for you

3-D printing offers innovative method to deliver medication

5 hours ago

3-D printing could become a powerful tool in customizing interventional radiology treatments to individual patient needs, with clinicians having the ability to construct devices to a specific size and shape. That's according ...

Mystery of the reverse-wired eyeball solved

Feb 27, 2015

From a practical standpoint, the wiring of the human eye - a product of our evolutionary baggage - doesn't make a lot of sense. In vertebrates, photoreceptors are located behind the neurons in the back of the eye - resulting ...

Neurons controlling appetite made from skin cells

Feb 27, 2015

Researchers have for the first time successfully converted adult human skin cells into neurons of the type that regulate appetite, providing a patient-specific model for studying the neurophysiology of weight ...

Quality control for adult stem cell treatment

Feb 27, 2015

A team of European researchers has devised a strategy to ensure that adult epidermal stem cells are safe before they are used as treatments for patients. The approach involves a clonal strategy where stem cells are collected ...

User comments : 0

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.