New research published in the February issue of the journal Nature Neuroscience found that an individual nerve cell in the prefrontal cortical (PFC) area can hold traces of memories on its own for as long as a minute, possibly even longer. Reseachers from the Department of Psychiatry at the University of Texas Southwestern Medical Center studying mice, found that rapid-fire inputs less than a second long initiate a cellular memory process in single cells lasting as long as minute, a process called metabotropic glutamate transmission. This transmission in the most highly evolved brain region holds moment-to-moment information.
This is the first study to identify the specific signal that establishes nonpermanent cellular memory and reveals how the brain holds temporary information. According to the authors, "it has implications for addiction, attention disorders and stress-related memory loss." Researchers have known that permanent memories are stored when the excitatory amino acid glutamate activates ion channels on nerve cells in the brain to reorganize and strengthen the cells' connections with one another. But this process takes minutes to hours to turn on and off and is too slow to buffer, or temporarily hold, rapidly incoming information.
The researchers identified in mice a specific metabotropic glutamate receptor (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 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.
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.
The study was funded by the National Institute on Drug Abuse; National Alliance for Research on Schizophrenia and Depression; the Alexander S. Onassis Public Benefit Foundation; and the Department of Veterans Affairs.
Sources:Posted by rsk at February 2, 2009 10:43 AM