The researchers identified in mice a specific metabotropic glutamate receptor called mGluR5 that, when turned on, starts a signaling cascade using calcium to hold a memory trace. This fast, short-term memory process happens inside individual cells; with long-term memory, additional proteins cause slow reorganization between cells in a network to establish a permanent memory.
Researchers examined brain cells from mice using nanoscale electrodes to measure the memory formation process.
To further understand how this short-term memory process relates to addiction, researchers applied the neurochemical dopamine to the memory buffer nerve cells. Dopamine is normally needed at an optimal level for an individual to focus attention and engage in fast decision-making memory, but drugs of abuse overload the brain with a surge of dopamine. In the study, researchers found that an experimental drug that activates a specific type of dopamine receptor "focused" the nerve cells, making the memory trace less susceptible to distraction.
When researchers employed an animal model of drug addiction using cocaine, they also found that repeated exposure to addictive levels of cocaine reduced memory trace activation in the memory buffer cells. When researchers then activated dopamine signaling in the "addicted" animals, essentially adding more dopamine to their systems, no focusing effect was observed.
"This makes sense because we know from human and animal models of addiction, when a decision using working memory has to be made, brain imaging shows a deficit in the same area of the brain we looked at," Dr. Cooper said. "It all fits together."
Researchers next plan to identify the ion channel responsible for holding and regenerating a memory trace. Their goal is to develop new pharmacological and genetic tools that will allow them to manipulate and possibly expand decision-making memory capacity.
"If we can identify and
|Contact: LaKisha Ladson|
UT Southwestern Medical Center