This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
A few weeks ago I blogged about a recent Nature paper which answered the question of how neurogenesis and stress can reciprocally regulate each other in mice. It's the kind of project that people in the field had been hypothesizing about and getting at indirectly for a long time, but it took a while to get to the actual experiments.
But now that laboratory is in gear, and already moving on, and today's poster looks at some of their latest work on HOW stress can change the survival of new neurons in your hippocampus.
Carter and Cameron. "Stress-induced modulation of glucocorticoid receptor expression in adult born neurons" Sunday AM poster session, 132.21, B31.
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The previous studies from the Cameron lab showed that ablating (getting rid of) neurogenesis in the hippocampus could alter the HPA axis, the interactions between the hypothalamus and pituitary and bodily responses that control how we respond to stress. But now we are looking at the opposite direction. Scientists have known for a while that chronic or acute physical stress can decrease the birth of new neurons (neurogenesis) in the hippocampus. In fact, we know that the stress hormone cortisol (corticosterone in rodents) is a regulator of neurogenesis. But HOW exactly does this occur?
To examine this question, the authors of this study want to look at how corticosterone receptors were changed in brand new neurons following stress. To do this, they injected mice with BrdU, a chemical that replaces thymidine when DNA copies itself, and then can be bound to an antibody which allows scientists to see it. Since it only works in copying DNA, it will label only cells that are in the process of replicating, and so if you look in the hippocampus, you'll only see the newest of neurons. You can then take those specific cells, and add another label which will look for the receptors GR (glucocorticoid) and MR (mineralocorticoid), which bind corticosterone.
So the authors gave BrdU and waited a week, and then exposed the animals to behavioral stress, either putting them in a new cage (a relatively mild stressor), or making them swim in a tank (a more severe stress). And then they looked to see how the new neurons responded, with what their GR and MR receptors looked like.
They found that swim stress, but not the exposure to the novel cage, increased glucocorticoid receptors in the week-old neurons in the hippocampus. There was no change in the mineralocorticoid receptors. So the stress, which increases corticosterone, increases glucocorticoid receptors in week old neurons.
What is the function of the increase glucocorticoid receptor expression? The scientists don't know yet, but this poster is the next tiny step in figuring out how stress and neurogenesis play nicely with each other, and what happens when they don't.
