From mice to men.

J Christian Althaus,Michael A Sutton

doi:10.7554/elife.67895

Abstract

All-trans retinoic acid induces functional and structural plasticity of synapses in human cortical circuits through the engagement of the spine apparatus.

Highlights

The researchers prepared slices from surgically resected brain tissue from patients undergoing neurosurgery to ask whether all-trans retinoic acid has the same effects on human pyramidal neurons from layer 2/3 of the cortex as it has on rodent neurons
Lenz et al demonstrated that the changes in synaptic strength induced by all-trans retinoic acid in human neurons depended on mRNA translation but not on transcription, a mechanistic signature first seen in rodent neurons
Lenz et al – who are based at the University of Freiburg and Goethe-University Frankfurt – explored the relationship between synaptic modulation by all-trans retinoic acid and the spine apparatus, an organelle that is present in a subset of dendritic spines and whose function has remained enigmatic (Jedlicka and Deller, 2017). They found that alltrans retinoic acid enlarged the spine apparatus and, strikingly, that the cross-sectional area of the spine apparatus varied with the size of the dendritic spine itself. This suggests that the spine apparatus might have a key role in the modulation of synaptic strength by all-trans retinoic acid

Summary

Introduction

All-trans retinoic acid induces synaptic plasticity in human cortical neurons. Synaptic signaling can either excite or inhibit the postsynaptic neuron, and the vast majority of excitatory synapses in the mammalian brain rely on structures called dendritic spines (Figure 1). Among the most promising of these is a derivative of vitamin A called all-trans retinoic acid, which can potently increase synaptic strength in cultured rodent neurons (Aoto et al, 2008).

Results

Conclusion