NMDA receptor activity stabilizes presynaptic retinotectal axons and postsynaptic optic tectal cell dendrites in vivo.
To investigate the role of N-methyl-D-aspartate (NMDA) receptor activity in the stability of the presynaptic axon arbor and postsynaptic dendritic arbors in vivo, we took time-lapse confocal images of single DiI-labeled Xenopus retinotectal axons and optic tectal neurons in the presence and absence of the NMDA receptor antagonist, APV. Retinotectal axons or tectal neurons were imaged at 30-min intervals over 2 h, or twice over a 24-h period. Retinal axons in animals exposed to DL-APV (100 microM) showed an increase in rates of branch additions and a decrease in branch lifetimes over 2 h compared to untreated axons. Under the same experimental conditions, tectal neurons showed a decreased rate of branch tip additions and retractions. APV treatment over 24 h had no apparent effect on axon arbor morphology, but did decrease tectal cell dendritic arbor elaboration. These observations demonstrate that NMDA receptor activity in postsynaptic neurons stabilizes pre- and postsynaptic neuronal morphology in vivo.. However, when NMDA receptor activity is blocked, presynaptic retinal axons respond with increased arbor dynamics while postsynaptic tectal cell dendrites decrease arbor dynamics. Such differential responses of pre- and postsynaptic partners might increase the probability of coactive afferents converging onto a common target under conditions of lower NMDA receptor activity.