A common neurotransmitter that conveys signals among brain cells reverses its normal function to accommodate new neurons in the brain. Since the remarkable 1998 discovery that people can grow new neurons well into old age, researchers have wanted to know how the newbies integrate themselves gracefully into existing neural networks without causing interference. Studies in embryonic rodents and monkeys suggested that the neurotransmitter GABA, which normally inhibits neurons from firing, may instead be stimulating young neurons to fire. Sparked by this clue, a group at Johns Hopkins University turned to a part of the hippocampus called the dentate gyrus. In a common strategy for visualizing new neurons, they introduced a retrovirus into mice that makes dividing neurons fluoresce green. They then measured the responsiveness of these cells to different neurotransmitters. Initially the new neurons were sensitive to GABA that had diffused into the space between cells. After a week the new cells connected to established neurons, which transmitted GABA in pulses. In another week the cells formed connections to receive glutamate, the major stimulatory neurotransmitter in adult neurons. The results indicate that despite differences between embryos and adults, “newly formed neurons must follow this sequence,” says Yehezkel Ben-Ari, director of the Mediterranean Institute of Neurobiology in France, who is not connected to the Johns Hopkins work. Apparently, an excess of chloride ions inside the young cells is responsible for their excitation by GABA. Chloride-deficient neurons that the scientists engineered showed a two-week delay in developing connections and eventually died. Johns Hopkins neuroscientist Hongjun Song says the team hopes to test whether applying GABA to stem cells at the right time and dose could help repair central nervous system injuries.
Since the remarkable 1998 discovery that people can grow new neurons well into old age, researchers have wanted to know how the newbies integrate themselves gracefully into existing neural networks without causing interference. Studies in embryonic rodents and monkeys suggested that the neurotransmitter GABA, which normally inhibits neurons from firing, may instead be stimulating young neurons to fire.
Sparked by this clue, a group at Johns Hopkins University turned to a part of the hippocampus called the dentate gyrus. In a common strategy for visualizing new neurons, they introduced a retrovirus into mice that makes dividing neurons fluoresce green. They then measured the responsiveness of these cells to different neurotransmitters.
Initially the new neurons were sensitive to GABA that had diffused into the space between cells. After a week the new cells connected to established neurons, which transmitted GABA in pulses. In another week the cells formed connections to receive glutamate, the major stimulatory neurotransmitter in adult neurons. The results indicate that despite differences between embryos and adults, “newly formed neurons must follow this sequence,” says Yehezkel Ben-Ari, director of the Mediterranean Institute of Neurobiology in France, who is not connected to the Johns Hopkins work.
Apparently, an excess of chloride ions inside the young cells is responsible for their excitation by GABA. Chloride-deficient neurons that the scientists engineered showed a two-week delay in developing connections and eventually died. Johns Hopkins neuroscientist Hongjun Song says the team hopes to test whether applying GABA to stem cells at the right time and dose could help repair central nervous system injuries.
