But OHSU researcher says jump in BDNF, neurogenesis may not be beneficial
PORTLAND, Ore. – Exercise enthusiasts have more reasons to put on their running shoes in the morning, but an Oregon Health & Science University scientist says they shouldn’t step up their work-outs just yet.
A study published today in the journal Neuroscience, journal of the International Brain Research Organization, confirmed that exercise increases the chemical BDNF – brain-derived neurotrophic factor – in the hippocampus, a curved, elongated ridge in the brain that controls learning and memory. BDNF is involved in protecting and producing neurons in the hippocampus.
“When you exercise, it’s been shown you release BDNF,” said study co-author Justin Rhodes, Ph.D., a postdoctoral fellow in the Department of Behavioral Neuroscience at OHSU’s School of Medicine and at the Veterans Administration Medical Center in Portland. “BDNF helps support and strengthen synapses in the brain. We find that exercise increases these good things.”
Mice bred for 30 generations to display increased voluntary wheel running behavior – an “exercise addiction” – showed higher amounts of BDNF than normal, sedentary mice. In fact, the BDNF concentration in the active mice increased by as much as 171 percent after seven nights of wheel running.
“These mice are more active than wild mice,” Rhodes said, referring to the mice as small and lean, and seemingly “addicted” to exercise. “Wheel running causes a huge amount of activity in the hippocampus. The more running, the more BDNF.”
In a study Rhodes also co-authored that extends these findings, to be published in the October edition of the American Psychological Association journal Behavioral Neuroscience, scientists demonstrated that not only do the mice display more of this “good” BDNF chemical in the hippocampus, they grow more neurons there as well.
But those high levels of BDNF and neurogenesis don’t necessarily mean an exercise addict learns at a faster rate, Rhodes said. According to the Behavioral Neuroscience study, the running addict, compared with the normal-running, control mice, perform “terribly” when attempting to navigate around a maze.
“These studies are focusing on the effects of exercise itself on chemicals known to protect and strengthen synapses,” Rhodes explained. “But too much of it is not necessarily a good thing.”
High runners tend to “max out” in the production of the BDNF and neurogenesis, Rhodes said. And that topping-out effect may be what prevents learning.
A high-running mouse’s inability to learn as well as a normal mouse could be due to less biological reasons, Rhodes points out. “It is possible that they’re so focused on running, they can’t think of anything else,” he said.
Rhodes and colleagues at the University of Wisconsin at Madison, the University of California at Riverside and The Salk Institute also emphasize that the functional significance of the exercise-induced increases in BDNF and neurogenesis is not known.
Rhodes suggests that when a high-running mouse exercises, stress is placed on its hippocampus and the development of new neurons becomes a protective response. No one has yet tested whether hyperactive wheel running exercise actually kills or damages neurons in the hippocampus, he said.
“The reason why these good things are happening is they may clean up some of the mess,” he said. “Knowing that, you wouldn’t expect high runners to get any benefit from it.”
One thing is clear: Exercise greatly activates the hippocampus. Rhodes and his colleagues have conducted research that also shows the intensity of exercise is linearly related to the number of neurons that are activated in a subregion of the hippocampus called the dentate gyrus.
In addition, they have demonstrated that when mice are kept from their normal running routine, brain regions involved in craving for natural rewards such as food, sex and drugs of abuse become activated. It is allowing Rhodes to study the relationship between natural craving, like hunger, and drug craving due to a pathological addiction.
“The point is to characterize what makes drug craving different from natural craving at the level of the genes and neuronal substrates involved so that, eventually, a pharmaceutical therapy can be designed to target the pathology,” Rhodes said.