To determine how GDF10 contributes to axonal sprouting, the researchers examined animal models of stroke and human autopsy tissue and discovered that GDF10 activates very early after stroke. They then tested the effect of GDF10 on the length of axons, which carry messages between brain cells, using animal and human neurons. They found that GDF10 stimulated axon growth and increased axon length.
The researchers also found that GDF10 may be important in recovery of motor function. Mouse models of stroke treated with GDF10 performed better in motor tasks and did not perform as well when GDF10 was blocked.
“These results indicate that the normal release of stroke-induced GDF10 participates in the limited motor recovery that occurs naturally in stroke,” wrote Dr Li. GDF10 is associated with much faster recovery after stroke, and levels of GDF10 in the brain are a signal of a need for recovery.
“We were surprised by how consistently GDF10 caused new connections to form across all of the levels of analysis,” said Dr Carmichael in a press release. “We looked at rodent cortical neurons and human neurons in dish as well as in live animals. It’s a demanding gauntlet to run, but the effects of GDF10 held up in all of the levels that we tested.”
The researchers also analyzed whether these repair mechanisms are similar to how the brain functions in early development. GDF10 was noted to affect entirely different genes than those affected in the development of learning and memory, meaning that after an injury, the regeneration in the brain is a unique process.
Li S, Nie EH, Yin Y, et al. GDF10 is a signal for axonal sprouting and functional recovery after stroke. Nature Neuroscience. 2015; doi:10.1038/nn.4146.