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The newspaper of The Johns Hopkins University August 6, 2007 | Vol. 36 No. 41
Researchers Find Another Clue Linking Addiction and Memory

By Nick Zagorski
Johns Hopkins Medicine

Our experiences — the things we see, hear or do — can trigger long-term changes in the strength of the connections between nerve cells in our brain, and these persistent changes are how the brain encodes information as memory. As reported in Neuron July 19, Johns Hopkins researchers have discovered a new biochemical mechanism for memory storage, one that may have a connection with addictive behavior.

Previously, the long-term changes in connection were thought to involve only a fast form of electrical signaling in the brain, electrical blips lasting about 100th of a second. Now, neuroscience professor David Linden and his colleagues have shown that another, much slower form of electrical signaling lasting about a second can also be persistently changed by experience.

They simulated natural brain activity by applying short electrical jolts to slices of rat brain and measuring the current flowing across the cells. After repeated jolting, the strength of the slow nerve signals had dramatically decreased and remained at a low intensity for 30 minutes after electrical jolts ceased.

These slow signals are produced by a nerve cell receptor called mGluR1, which has been associated with behaviors such as addiction and epilepsy.

"Both of these conditions also involve long-term changes in the function of nerve connections,  Linden said. "So in addition to furthering our basic understanding of memory storage, our work suggests that drugs designed to alter mGluR1 are promising candidates for the treatment of addiction, epilepsy and diseases of memory. 

The research was funded by the Republic of Korea Ministry of Health and Welfare and the National Institutes of Health.

Authors on the paper are Paul Worley and Linden, of Johns Hopkins; and Sang Jeong Kim, Yunju Jin and Jun Kim, of Seoul National University College of Medicine.


Related Web sites

David Linden
'Neuron '


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