Aim: 

Amyotrophic lateral sclerosis (ALS) is a devastating progressive neurodegenerative disorder involving primarily motor neurons of cerebral cortex, brain stem and spinal cord. Agonists acting at group II metabotropic glutamate (mGlu2/3) receptors are now considered potential drugs in acute and chronic neurodegeneration, by promoting the synthesis and release of neurotrophic factors in astrocytes. Here, we studied the different distribution of mGlu2/3 receptors in the spinal cord of control and G93A-SOD1 mice.

Methods: 

Double-labeling immunofluorescence and confocal analysis were performed on spinal cord sections of wild type mice (WT), and transgenic mice expressing high levels of the human mutated protein G93A SOD-1, an animal model of ALS.

Results: 

In WT and G93A-SOD1 mice, mGlu2/3 receptors were clearly expressed in the dorsal horn of spinal cord, several scattered neurons of the ventral horn and ependimal cells. Double-labeling experiments revealed that mGlu2/3 immunoreactivity was present in motor neurons, parvalbumin and calbindin positive neurons. Interestingly, in G93A-SOD1 mice, mGlu2/3 receptors were present in many surviving neurons and appeared to be overexpressed in reactive astrocytes.

Conclusion: 

Our data suggest that the presence of mGlu2/3 receptors might foster neuronal survival. In addition, the upregulation of mGlu2/3 receptors in reactive astrocytes of G93A mice might exert a neuroprotective effect during ALS progression.