Translational Control of Synaptic Plasticity and Memory - Biophysical Approaches to Translational Control of Gene Expression - page 284

Chapter 14
Translational Control of Synaptic Plasticity
and Memory

Arkady Khoutorsky , Christos Gkogkas, and Nahum Sonenberg

14.1 Introduction

Synaptic plasticity refers to the ability of neurons to change synaptic transmission
efficiency in response to specific stimuli. Different stimuli lead to either enhance-
ment or depression of synaptic strength. In mammals, activity-dependent long-
lasting enhancement of synaptic strength is called long-term potentiation (LTP),
whereas a long-lasting decrease in synaptic efficiency is referred to as long-term
depression (LTD). LTP exhibits two temporally distinct phases that are defined by
their requirement for new gene expression: early-phase LTP (E-LTP) does not
depend on protein synthesis, but relies on modification of preexisting components,
whereas late-phase LTP (L-LTP) requires transcription and synthesis of new pro-
teins. LTP is generally considered to be the cellular model for learning and memory,
as both LTP and memory share similar molecular and cellular mechanisms. Similarly
to LTP, memory formation presents two temporal phases with respect to their
requirement of new gene expression. Short-term memory (STM) lasts minutes to
hours and does not require the synthesis of new proteins, while long-term memory
(LTM) lasts days or even a lifetime and is heavily dependent on the generation of
new proteins (Abel et al. 1997 ; Kandel 2001 ) .
Newly synthesized proteins contribute to structural changes that accompany
long-lasting synaptic plasticity and memory. Synaptic stimulation induces the for-
mation of new spines (Desmond and Levy 1983 ; Toni et al. 1999 ) , and promotes
protein synthesis-dependent enlargement of existing spines (Tanaka et al. 2008 ) .
These morphological changes are also observed after behavioral training (Ramirez-
Amaya et al. 1999, 2001 ; Leuner et al. 2003 ) .