Can quantum dots shed some light on how we remember stressful events?
David L. Shenkenberg
In dangerous situations, our bodies enter the fight-or-flight mode, in which our heart rate increases, we breathe more rapidly, and we feel less pain, among many other changes. Although most of us do not regularly face life-and-death situations, we do regularly experience stressful events that send our bodies into this fight-or-flight mode.
Hormones are what signal the body to enter this mode. Once one of these hormones, called corticosterone, reaches the structure of the brain called the hippocampus, it causes neural changes that need further investigation. Because the hippocampus is responsible for human learning and memory, these neural changes could help us store memories of stressful situations so that we can avoid them or respond better to them in the future.
Researchers from the University of Bordeaux 2 in France have shown how corticosterone likely prepares AMPA receptors in the hippocampal brain cells to receive glutamate, the ubiquitous excitatory neurotransmitter. They studied brain cells from the hippocampi of rats. They labeled AMPA receptors that receive glutamate in these brain cells with antibody-conjugated quantum dots, and they tracked individual quantum dots in and around the brain cells using an ordinary wide-field microscope and a Photometrics electron-multiplying CCD camera.
Researchers added the stress hormone corticosterone to hippocampal neurons and tracked the AMPA receptor using antibody-conjugated quantum dots.
They found that corticosterone increases the availability of these receptors beyond the synapse, the space between brain cells where electrical and chemical signals shoot out.
“These receptors have been highly studied over the last decades because they are the basis of the molecular mechanisms involved during synaptic plasticity,” explained lead researcher Laurent Groc. “What we uncovered in this study is that the surface trafficking of the AMPA receptor is a likely target of the stress hormones, opening avenues for drug targeting.”
Nature Neuroscience, August 2008, pp. 868-870.
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