Using a recording technique from the ventral roots of the isolated hemisected baby rat spinal cord, the action of mGluRs agonists has been studied on postsynaptic motoneurons membrane potential when applied alone or in combination with NMDA. The mGluRs group I/II selective agonist 1S,3R-ACPD (1-100μM) by itself caused a dose dependent depolarization of motoneurons which was blocked in a competitive manner by ( S )-4-CPG (an antagonist for group I mGLURs) and by (+)MCPG (an antagonist for group I and II mGluRs). The agonist-induced depolarization is probably attributable to the activation of group I mGluRs since the group I specific agonist DHPG (1-100μM) produced a dose dependent depolarization of the neonatal motoneurons, while the group II and III specific agonists L-CCG-I and L-AP4 did not. Both 1S,3R-ACPD and DHPG were able to increase NMDA depolarization in a dose dependent manner. 1S,3R-ACPD (10μM) and DHPG (30μM) potentiated the NMDA (10μM) induced-depolarization by 37% and by 26%, respectively. In contrast, the group II selective agonist L-CCG-I had no significant effect on the depolarization of motoneurons evoked by application of NMDA. The potentiation of the NMDA response elicited by 10μM 1S,3R-ACPD was completely blocked (100%) by coapplication of the group I selective antagonist (S)-4CPG (1mM).These results suggest that the mGluRs of the PI-linked family are able to depolarize the membrane potential of the motoneurons as well as to potentiate the NMDA induced-depolarization.