This is indeed an interesting paper. If neuronal maturation in primates takes so much longer than in rodents, this has many implications. The current idea is that there is a time window during this maturation when new cells are particularly sensitive. They are more excitable and show a reduced threshold for synaptic plasticity; their level of LTP is elevated. It has been reported that essentially all LTP that can be elicited in the dentate gyrus under normal conditions is coming from the immature new neurons. The remainder of the neurons, the mature ones, are heavily inhibited. This physiological aspect is not studied here, but the authors examined a number of morphological signs of maturation. The data might indicate that primates have relatively more cells in this critical period because the individual cells remain there longer. This, indeed, has implications for many functional considerations, including the potential role of neurogenesis in depression and antidepressant treatment.

However, the idea that new neurons would be antidepressants because they replace missing...  Read more

This is indeed an interesting paper. If neuronal maturation in primates takes so much longer than in rodents, this has many implications. The current idea is that there is a time window during this maturation when new cells are particularly sensitive. They are more excitable and show a reduced threshold for synaptic plasticity; their level of LTP is elevated. It has been reported that essentially all LTP that can be elicited in the dentate gyrus under normal conditions is coming from the immature new neurons. The remainder of the neurons, the mature ones, are heavily inhibited. This physiological aspect is not studied here, but the authors examined a number of morphological signs of maturation. The data might indicate that primates have relatively more cells in this critical period because the individual cells remain there longer. This, indeed, has implications for many functional considerations, including the potential role of neurogenesis in depression and antidepressant treatment.

However, the idea that new neurons would be antidepressants because they replace missing cells is unlikely to be true. There has been a number of arguments against neurogenesis explaining the delay between the initiation of antidepressant medication and the detection of positive effects, including one we recently published (see Klempin et al., 2010). The more important thing is that primates might have plastic new neurons for a longer time than rodents. The details will have to be ironed out, including the physiology, which will be crucial but hard to get from primates.

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