A dendrodendritic reciprocal synapse provides a recurrent excitatory connection in the olfactory bulb -- Data Supplement - Supplemental Data -- Proceedings of the National Academy of Sciences

Supplementary material for Didier et al. (May 15, 2001) Proc. Natl. Acad. Sci. USA, 10.1073/pnas.101126398

Supplemental Figure 8 Fig. 8.
Both APV-sensitive and APV-resistant NMDA currents are present at the dendro-dendritic reciprocal synapse. (A) Model showing the effect of the drugs onto the receptors and the depolarization evoked response. Standard conditions are NBQX and BMI-PTX in the bath. APV blocks only the NMDA receptors present on granule cell terminals that in turn stop the glutamate release. The NMDA receptors on the mitral cell could still be activated either through glutamate autodetection or exogenous glutamate application. In the presence of APV, bath application of dCK antagonizes the remaining NMDA receptors. (B) Iontophoretic application of glutamate revealed that APV is almost ineffective (cell recorded in 0 Mg²⁺, TTX, BMI, PTX, strychnine, and NBQX). In fact, APV induces a slight potentiation of the iontophoretic response. However, normalization of the responses either on their maximal amplitude (scaling 1) or on their onset (scaling 2) revealed an APV-sensitive component. The glutamate application will act directly on the mitral cell secondary dendrite but also on the granule cell spine that will release glutamate. Thus, APV prevents this glutamate release from granule cell. (C) Puff of NMDA (0.5 mM) revealed also the presence of APV-resistant NMDA receptor on the mitral cell lateral dendrites. (C1) A short application of NMDA (25 ms) displayed a response that was almost due to APV-resistant NMDA receptor. (C2) Longer application (100 ms) revealed a biphasic response. APV application blocked the late phase of the response. All cells were recorded in 0 Mg²⁺, TTX, BMI, PTX, and NBQX and voltage clamped at –60 mV.