Structural plasticity of dendritic spines

Abstract

Dendritic spines are small mushroom-like protrusions arising from neurons where most excitatory synapses reside. Their peculiar shape suggests that spines can serve as an autonomous postsynaptic compartment that isolates chemical and electrical signaling. How neuronal activity modifies the morphology of the spine and how these modifications affect synaptic transmission and plasticity are intriguing issues. Indeed, the induction of long-term potentiation (LTP) or depression (LTD) is associated with the enlargement or shrinkage of the spine, respectively. This structural plasticity is mainly controlled by actin filaments, the principal cytoskeletal component of the spine. Here we review the pioneering microscopic studies examining the structural plasticity of spines and propose how changes in actin treadmilling might regulate spine morphology.

Figure 1. Actin filaments in the dendritic spine

(A) Expansion of the dendritic spine and rapid polymerization of actin by local tetanic stimulation. Actin polymerization was visualized by FRET-based imaging method, which detects the proximity of actin molecules. Obtained from [47]. (B) An electron micrographic image of a dendritic spine showing S1-fragment labeled F-actin. Contrast was adjusted from the original and coloring (red, spine head; yellow, dendritic shaft) was added by the authors of this review. Arrowheads point to the spine neck. Obtained from [12].

Figure 2. Proposed mechanisms for spine expansion

(A) In a naive spine, there is a constant treadmilling of actin from the periphery to the center of the dendritic spine, maintained by an equilibrated rate of F-actin polymerization/depolymerization. (B) LTP induction stabilizes the actin filaments and slows down the depolymerization at the pointed end of F-actin located at the core of dendritic spine. (C) Polymerization continues in the periphery of dendritic spine, thereby generating the driving force that expands the spine head.