The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 4 • January 2016


Like any physiological process, there is a level at which too much neurogenesis can lead to adverse effects (Hsieh and Schneider, 2013). The effects of various levels of electrical activity on neurogenesis have been described (Hsieh and Schneider, 2013) as follows: “It may be that the neurogenesis response of stem progenitor cells to [electrical] activity is an adaptive mechanism to maintain regional homeostasis: increasing stem cell production when local circuitry activity levels are low, and restoring quiescence when activity levels are high.” The point here is that when activity levels are too high, you have electrical activation that becomes pathologically high as occurs during an epileptic seizure. As the authors go on to explain: “A potential ‘cost’ of excitable stem cells is inappropriate activation after pathological forms of activity, such as seizures.”

The authors also describe a possible excitation signal as follows: “A possible mechanism for excitation-neurogenesis coupling is GABA-mediated depolarization, previously described in mouse embryonic neuronal progenitor cells. Depolarization causes an increase in intracellular Ca2+ concentration similar to that evoked in cultured neural stem/progenitor cells. This excitation signal is relayed to the genome wherein the transcription factor NeuroD is rapidly activated to promote neurogenesis.” “...excitation signaling in the form of GABA is also necessary to drive the functional integration of newborn neurons.”

In another paper (Veyrac, 2013), the authors explain, “Newborn DGCs [dentate granule cells] are initially tonically activated by ambient depolarizing GABA....” Following hyperpolarization (by process that includes expression of glutamate receptors), “...they are hyperexcitable, display properties of ehanced synaptic plasticity, and are prone to integrate the existing hippocampal neurocircuitry.”

Importantly, the authors point out, “As their functional maturation progresses, however, newborn DGCs compete to survive, leaving the majority eliminated by cell death. Several behavioral manipulations, in particular hippocampal dependent learning, can regulate their rate of survival.” In this paper (Veyrac, 2013), the authors identify the Zif268/egr1 gene as controlling the selection, maturation, and functional integration of adult hippocampal newborn neurons by learning.”

Immediate Early Genes Are Transiently And Preferentially Induced In Newborn DGCs During Their Critical Period Of Maturation

Zif268/egr1 is one such immediate early gene and, as explained in the paper, actively controls the survival of newborn DGCs during their critical period of maturation in the first 2-3 weeks of their birth.”

The requirement for excitation during the early phase of newborn neuronal maturation may be a reason that the decline in arachidonic acid in cell membranes of the brain with aging is a negative factor in cognition (McGahon, 1997). Despite the fact that the metabolic products created by arachidonic acid are often involved in damage due to excessive inflammation, arachidonic acid is there for some reason(s) and this might be one of those reasons. Rice oil is relatively rich in arachidonic acid. Perhaps this is one reason that the Japanese who live in Japan, who consume a lot of rice and use rice oil in cooking, may live longer than those in other countries.

DHA Protects the Brain Against Inflammation

As we have written before, one way to protect the brain against arachidonic acid-associated inflammation is to take supplementary DHA, docosahexaenoic acid, as found in fish oils. (Basselin, 2012).


  • Hsieh and Schneider. Neural stem cells, excited. Science. 339:1534-35 (2013).
  • Veyrac, Gros, Bruel-Jungerman, et al. Zif268/egr1 gene controls the selection, maturation and functional integration of adult hippocampal newhorn neurons by learning. Proc Natl Acad Sci U S A. 110(17):7062-67 (2013).
  • McGahon, Clements, Lynch. The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed. Neuroscience. 81(1):9-16 (1997).
  • Bresselin, Ramadan, Rapoport. Imaging brain signal transduction metabolism via arachidonic acid and docosahexaenoic acid in animals and humans. Brain Res Bull. 87(2-3):154-71 (2012).

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