Mechanisms Mediating Brain Plasticity: IGF1 and Adult Hippocampal Neurogenesis

This review addresses the role of serum insulin-like growth factor 1 (IgF1) as one mechanism of adult neural plasticity, specifically, its regulation of hippocampal neurogenesis among other plasticity-related processes. It is suggested that IgF has been reused advantageously both for the control of energy expenditure as a function of the organism's activity and to protect, repair, and plastically modulate the brain. Moreover, because as the main source of IgF1 in the adult organism is outside the brain and its presence in this organ is a function of the activity, IgF1 becomes an ideal factor to induce plastic/neuroprotective functions as a function of the organism's activity. The link for this point of view comes from the original function of IgF1 during ontogeny/phylogeny, the promotion of cell survival and control of neural cell numbers, whereas one of the IgF1 functions in the adult brain is the control of hippocampal neurogenesis. The investigation of the IgF1 role as mediator of exercise effects suggests that many but not all the effects of physical activity are mediated by IgF1. These investigations have contributed to delimit the role of IgF1 as mediator of exercise actions, but at the same time are unveiling new roles for serum IgF1 inside the brain.