Brain activity requires a flux of glucose to active regions to sustain increased metabolic demands. Insulin, the main regulator of glucose handling in the body, has been traditionally considered not to intervene in this process. However, we now report that insulin modulates brain glucose metabolism by acting on astrocytes in concert with IGF-I. The cooperation of insulin and IGF-I is needed to recover neuronal activity after hypoglycemia. Analysis of underlying mechanisms show that the combined action of IGF-I and insulin synergistically stimulates a mitogen-activated protein kinase/protein kinase D pathway resulting in translocation of GLUT1 to the cell membrane through multiple protein-protein interactions involving the scaffolding protein GAIP-interacting protein C terminus and the GTPase RAC1. Our observations identify insulin-like peptides as physiological modulators of brain glucose handling, providing further support to consider the brain as a target organ in diabetes.

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The influence of the learning process on the persistence of the newly acquired behavior is relevant both for our knowledge of the learning/memory mechanisms and for the educational policy. However, it is unclear whether during an operant conditioning process with a continuous reinforcement paradigm, individual differences in acquisition are also associated to differences in persistence of the acquired behavior. In parallel, adult neurogenesis has been implicated in spatial learning and memory, but the specific role of the immature neurons born in the adult brain is not well known for this process. We have addressed both questions by analyzing the relationship between water maze task acquisition scores, the persistence of the acquired behavior, and the size of the different subpopulations of immature neurons in the adult murine hippocampus. We have found that task acquisition and persistence rates were negatively correlated: the faster the animals find the water maze platform at the end of acquisition stage, the less they persist in searching for it at the learned position in a subsequent non-reinforced trial; accordingly, the correlation in the number of some new neurons' subpopulations and the acquisition rate is negative while with persistence in acquired behavior is positive. These findings reveal an unexpected relationship between the efficiency to learn a task and the persistence of the new behavior after a non-reinforcement paradigm, and suggest that the immature neurons might be involved in different roles in acquisition and persistence/extinction of a learning task. © 2016 Wiley Periodicals, Inc.

Doublecortin (DCX)‐Calretinin (CLR) immunolabeling of the hippocampal dentate gyrus of a 4 month old male mice (Mus musculus). DCX+ (red) and CLR+ (green) neurons in a section from a control (no treatment) mouse, where both DCX+/CLR+ and DCX+/CLR+ can be appreciated. This dual labeling lets to count two different subpopulation of immature, differentiating neurons in two successive stages of maturation with one double immunohistochemistry reaction. Cell counts were performed in these type of sections by using the U‐disector and confocal microscopy. The cover image, by J.L. Trejo et al., is based on the Research Article The relationship between behavior acquisition and persistence abilities: Involvement of adult hippocampal neurogenesis, DOI: .