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

Supplemental Figure 7

Fig. 7.

Characterization of APV-resistant NMDA receptors on mitral cell lateral dendrites. (A) Superimposed current traces illustrating the responses evoked by glutamate iontophoresis in the absence (black) or the presence of 100 µM D,L-APV (red) when cells were recorded in 0 Mg2+, TTX, BMI, PTX, strychnine, and NBQX. (B) Summary graph showing the relationship between amplitude of iontophoretic responses vs. the ejecting current intensity measured from eight different experiments. Note the homogeneous potentiation of the control curve (Ctrl, black dots) induced by APV (red dots) all over the range of stimuli. The dotted line represents control values multiplied by a scaling factor corresponding to a potentiation of about 20%. (C) Traces representing a single experiment in which the concentration of d,l-APV was increased. Concentration of d,l-APV up to 700 µM did not block the iontophoretic response later identified as NMDA current with dCK (15 µM). A small potentiation of the response was observed for APV concentrations ranging from 100 to 300 µM. The cell is recorded in the same condition as in A. (D) Summary graph of seven different experiments showing that APV (up to 700 µM) does not reduce the response when compared to the control recorded in the absence of APV. In all of these experiments, cells were voltage-clamped at -60 mV. Altogether, these results rule out the possibility that APV, a competitive antagonist, was inefficient because of a massive application of exogenous glutamate.