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The [2,3]‐sigmatropic rearrangement, constitutes a versatile type of bond reorganization which encompasses a number of variations in terms of an atom pair (X, Y) and the type of electron pair on Y (anions, nonbonding electron pairs, or ylides). The Sommelet–Hauser rearrangement is representative. This chapter focuses on the special class of [2,3]‐sigmatropic rearrangement that involves an oxycarbanion (X = oxygen, Y = carbanion) as the migrating terminus. This type of rearrangement is now termed the [2,3]‐Wittig (sigmatropic) rearrangement. The reaction name clearly originates from the fact that this rearrangement formally represents a [2,3]‐sigmatropic version of the classic Wittig rearrangement, a well‐known 1,2‐alkyl shift of oxycarbanions. The [2,3]‐Wittig rearrangement has a rather recent history. Perhaps the first observation of the [2,3]‐Wittig shift is the rearrangement of the allyl fluorenyl ether, which was made in 1960 in the context of mechanistic studies on the Wittig rearrangement. The period of the 1960s to the early 1970s witnessed slow progress with a focus on mechanistic studies mainly of allyl benzyl ether systems. The synthetic power of this carbanion rearrangement as a general method was recognized when Still (1978) and Nakai (1981) established the highly stereoselective variants of the genuine [2,3]‐Wittig rearrangement. In recent years the [2,3]‐Wittig rearrangement has enjoyed widespread application in many facets of organic synthesis. Various aspects of the reaction have been reviewed. This chapter deals with the mechanism, scope and limitation, stereochemistry, and synthetic applications of the [2,3]‐Wittig rearrangement with emphasis on the stereochemical aspects and the synthetic utility. Other hetero [2,3]‐Wittig rearrangements such as thio‐[2,3]‐Wittig variants are not covered.

Synaptic plasticity in hippocampal neurons has been thought to represent a variety of memories. Although accumulating evidence indicates a crucial role of BDNF/TrkB/Akt signaling in the synaptic plasticity of the hippocampus, the mechanism by which Akt, a serine/threonine kinase, controls activity-dependent neuronal plasticity remains unclear. Girdin (also known as APE, GIV, and HkRP1), an actin-binding protein involved both in the remodeling of the actin cytoskeleton and in cell migration, has been identified as a substrate of Akt. Previous studies have demonstrated that deficit of neuronal migration in the hippocampus of Girdin-deficient (Girdin Ϫ/Ϫ ) mice is independent on serine phosphorylation of Girdin at S1416 (Girdin S1416) by Akt. In the present study, we focused on the role of Girdin S1416 phosphorylation in BDNF/TrkB/Akt signaling associated with synaptic plasticity. We found that Girdin in the hippocampus was phosphorylated at S1416 in an activity-dependent manner. Phosphorylation-deficient knock-in mice (Girdin SA/SA mice), in which S1416 is replaced with alanine, exhibited shrinkage of spines, deficit of hippocampal long-term potentiation, and memory impairment. These phenotypes of Girdin SA/SA mice resembled those of Girdin ϩ/Ϫ mice, which have 50% loss of Girdin expression. Furthermore, Girdin interacted with Src kinase and NR2B subunit of NMDA receptor, leading to phosphorylation of the NR2B subunit and NMDA receptor activation. Our findings suggest that Girdin has two different functions in the hippocampus: Akt-independent neuronal migration and Akt-dependent NR2B phosphorylation through the interaction with Src, which is associated with synaptic plasticity in the hippocampus underlying memory formation.