Cellular and Molecular Neurobiology
Author: Rocio Gutierrez Fuster | email: rgutierrezfuster@iib.unsam.edu.ar
Rocio Gutiérrez Fuster 1°, Antonella Leon 1°, Gabriela Ines Aparicio 1°, Rodrigo Herrera Molina 2°, Camila Scorticati 1°
1° Instituto de Investigaciones Biotecnológicas, Universidad Nacional de San Martín (UNSAM) Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) , San Martín, Buenos Aires, Argentina
2° Center for Behavioral Brain Sciences, Magdeburg, Germany
The molecular mechanisms underlying structural neuronal plasticity are not completely understood. In this regard, neuronal membrane glycoprotein M6a induces structural plasticity through mechanisms that have not been fully established yet. The relevance of studying the mechanisms by which M6a promotes neuronal plasticity raised from existing variants of the GPM6A gene or inadequate expression levels linked to neuropsychiatric disorders, such as schizophrenia, depression, Alzheimer and claustrophobia. Since the extracellular loops of M6a (ECs) command its function, previous results from our laboratory determined that cellular adhesion molecules (CAMs) neuroplastin (NPTN) and the intercellular adhesion molecule ICAM5 are candidates to interact with the ECs of M6a and modify its function. Here, we aimed to study the possible physical-functional association of M6a, NPTN and ICAM5 in hippocampal culture neurons and cell lines. Both ICAM5 and NPTN colocalize in cis with M6a at the membrane of culture neurons. Also, both CAMs colocalize with M6a in cis and trans in N2a and HEK293 cells. Hippocampal neurons co-expressing M6a/ICAM5 showed significantly higher filopodia number compare to neurons overexpressing M6a or ICAM5 alone. By contrast, in M6a/NPTN co-expressing neurons filopodia density significantly decrease. Together, even though both CAMs colocalize with M6a at the neuronal membrane, ICAM5 acts synergistically and NPTN antagonistically.