Glutamate receptor activity is required for normal development of tectal cell dendrites in vivo.

Glutamatergic retinotectal inputs mediated principally by NMDA receptors can be recorded from optic tectal neurons early during their morphological development in Xenopus tadpoles. As tectal cell dendrites elaborate, retinotectal synaptic responses acquire an AMPA receptor-mediated synaptic component, in addition to the NMDA component. Here, we tested whether glutamatergic activity was required for the elaboration of dendritic arbors in Xenopus optic tectal neurons. In vivo time-lapse imaging of single DiI-labeled neurons shows that the NMDA receptor antagonist APV (100 microM) blocked the early development of the tectal cell dendritic arbor, whereas the AMPA receptor antagonist CNQX (20 microM) or the sodium channel blocker TTX (1 microM) did not. The decreased dendritic development is attributable to failure to add new branches and extend preexisting branches. These observations indicate that NMDA-type glutamatergic activity promotes the initial development of the dendritic arbor. At later stages of tectal neuron development when AMPA receptor-mediated synaptic transmission is strong, both APV and CNQX decrease dendritic arbor branch length, consistent with a role for glutamatergic synaptic transmission in maintaining dendritic arbor structure. These results indicate that AMPA and NMDA receptors can differentially influence dendritic growth at different stages of neuronal development, in correlation with changes in the relative contribution of the receptor subtype to synaptic transmission.