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May 28

Molecular Memory

Memory & Forgetting: The Molecular Puzzle

Below is summary of an interesting article I recently read discussing the molecular composition of memory. Published by the Dana Foundation (, a private philanthropic organization that supports brain research through grants and educates the public about the successes and potential of brain research, I found the article helpful because of its succinct nature condensing the most up-to-date neuro scientific molecular research relating to memory. If interested in expanding your knowledge in this field, I encourage you to sign up for their monthly newsletter.


Memory and Forgetting: Piecing Together the Molecular Puzzle of Memory Storage

The 2010 Progress Report on Brain Science

By Sandra A. Swanson


1. Cyclic-AMP response element-binding protein, or CREB. In early studies involving fruit flies and sea slugs, CREB is identified as having a role in converting short-term memories to long-term ones. Studies in the mid-1990s have already suggested a basic difference in the molecular mechanisms of short-term versus long-term memories, namely that long-term memories do require protein synthesis, while short-term memories do not require a molecular conversion.

2. Recent research has indicated that fear memories can be rapidly erased and that specific proteins have significant powers to abolish them.

In October 2008, neurobiologist Joe Tsien published a paper that demonstrated the selective deletion of fear memories in mice. He and his researchers found that when the protein alpha-CaM kinase II was over expressed in mice during memory recall, it could erase both short-term and long-term fear memories.

One of the most promising results focused on targeted nature of this memory deletion. Tsien and his colleagues found that when alpha-CaM kinase II was overexposed, the memory being retrieved was the only one affected-other fear memories in the mice remained intact.

3. In March 2009, Sheena Josselyn and her colleagues at the University of Toronto set out to identify the neurons that support a particular memory. What they found was that instead of congregation in a certain areas or sections of the brain, the neurons linked to a specific memory tend to be scattered throughout a brain region.

Josselyn used an experiment that trained mice to fear a tone. Her previous work had suggested that when auditory fear memories form, they tend to recruit amygdala neurons with high levels of CREB. After mice received the toxin that deletes neurons with high CREB levels, the animals stopped fearing the tone. However, this did not impair the animal’s overall capacity for learning. They continued to encode new memories after the toxin destroyed specific CREB-rich neurons.

4. James McGaugh at the University of California-Irvine demonstrates that memories can be artificially altered when they are recalled, or remembered by administering a substance called propanolol (Inderal). This is possible through a process called reconsolidation-when a memory is retrieved, it temporarily loses stability and can be strengthened or weakened. Propanolol (Inderal) has been approved by the FDA as a blood-pressure drug; musicians and other performers have also used Inderal to combat stage fright.

5. Merel Kind and her fellow researchers at the University of Amsterdam published a paper in March 2009 with human subjects that focused on the erasure of only the emotional component of the memory and not the complete memory. Kind created a fear memory by showing his subjects photographs of spiders and then administering a mild eclectic shock. After the subjects had been conditioned to associate spider images with shocks, half of them received a dose of propranolol. Next, all of the subjects were exposed again to the spider photos and the shocks, reactivating the memory. The result: subjects who received propranolol showed a loss of fear response. The drug dulled the emotional component but did not delete the memory of the experience. The subjects’ declarative memory, which encompasses facts and events, remained intact.

Why? The propranolol blocks adrenaline receptors concentrated in the amygdala, where fear memories are believed to be stored causing hindrance in the reconsolidation of fear memories.

6. Joe Tsien’s research has shown that the duration of short term-memory, long recognized as particularly vulnerable to change and easily weakened, can be altered when overexposure to a protein and that the timing is critical.

When researchers elevated the protein alpha-CaM kinase II within ten minutes of engaging mice in a learning activity, it stunted short-term memory formation. But when the protein alteration took place fifteen minutes after the learning activity, it did not result in a disruption of short-term memory.

7. Todd Sacktor and his colleagues at SUNY Down State Medical Center published a paper in 2006 suggesting that the enzyme PKN zeta was needed to maintain long-term memory. “It used to be thought that long-term memory was due to structural changes in the brain that were permanent because they were structural,” said Sacktor. “The idea was that once you make a synapse, that’s it-you can forget about the memory maintenance part.”

In 2009, Sacktor followed-up his previous showing that PKM zeta is an integral part of long-term memory upkeep. His research was able to delete three-month old memories in rats, but found that inhibiting PKM zeta had no effect on short-term memory.

8. According to a study published in October 2008, a molecule called myosin Vb may be indispensable to the structural and functional changes necessary for plasticity, the brain’s ability to rewire neuron connections in response to an experience. Researchers have observed that the myosin molecule facilitates the movement of new receptors in a rodent’s hypothalamus, which in turn strengthens synaptic connections. When myosin was blocked, it prevented the addition of new receptors.

In August 2008, scientists have also identified a protein that triggers plasticity in visual systems. The protein orthodenticle homeobox 2, or Otx2, facilitates the maturation of cells located in certain visual cortex, which helps rewire the brain in response to visual input.



Read April's Ed Tip to understand how using video game design principles will improve instruction.  Moreover, educators should not view video games as the enemy of education, but rather a model for best teaching practices. When educators design instructional strategies, they must keep in mind the principles of video games, namely achievable challenge, and the role of dopamine in education.