University of Southern California neuroscientists have found a chemical mechanism that explains how estrogen enhances the process believed responsible for memory.
"Previous studies have suggested that the hormone estrogen delays the onset of Alzheimer's disease, and several million post-menopausal women are taking estrogen supplements for that reason," says USC neurophysiologist Richard F. Thompson, Ph.D. "Our research reveals a chemical mechanism that could explain how the delay in onset occurs."
Dr. Thompson and his colleagues measured the excitability and long-term potentiation between neurons from the brain of a rat, both before and after exposing slices of the brain's hippocampus to estrogen. The researchers looked specifically at the hormone's influence on a neurotransmitter called glutamate and two of its receptors, NMDA and AMPA. Neurotransmitters are chemicals that mediate the transmission of electrical impulses across the synapses between neurons.
"The estrogen activated both receptors within minutes -- causing a lasting increase in neuronal activity," Thompson reports. "Estrogen also enhanced the process of long-term potentiation. Activating the NMDA receptor apparently initiates long-term potentiation, and the AMPA receptors maintain it."
Since its discovery more than two decades ago, long-term potentiation has been intensively studied in hundreds of research laboratories around the world. The phenomenon is a long-lasting increase in neuronal responses in the hippocampus, a major structure in the forebrain of all mammals. It is thought to be a mechanism of memory shortage in the brain.
Thompson believes that learning more about the mechanism of long-term potentiation could lead to highly refined treatments for Alzheimer's disease. Researchers are studying compounds that are similar or related to estrogen in the hope of finding a drug precisely targeted for the treatment of disease while avoiding unwanted side-effects.
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Contact: Bob Calverley
calverle@usc.edu
213-740-4750
University of Southern California
17-Mar-1999