The Journal of Neuroscience, January 5, 2005, ():
Mechanisms Underlying Developmental Speeding in AMPA-EPSC Decay Time at the Calyx of Held
J. Neurosci. Koike-Tani et al.
25: 199
Supplemental data
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Supplementary Figure 1 Expression of GluR2 protein in MNTB principal neurons at P7. A, Immunofluorescence staining of an MNTB neuron with a GluR2 antibody (in green, left panel) and with a synaptophysin antibody as a synaptic marker (in red, middle panel), and merged picture (right panel). Mouse monoclonal anti-GluR2 antibody (Chemicon, Temecula, CA; diluted 1:100) and rabbit polyclonal anti-synaptophysin antibody (Zymed, South San Francisco, CA; diluted 1:100) were used. GluR2 and synaptophysin were visualized using the goat secondary antibodies conjugated with Alexa fluor 488 and Alexa fluor 568 (Molecular Probes; Eugene OR, diluted 1:200), respectively. Stained sections (30 µm in thickness) were viewed with a 100X oil-immersion objective (numerical aperture 1.35) using a confocal laser scanning microscopy(Fluoview FV300; Olympus Optical) with argon and krypton laser. B, The current-voltage relationships of nerve evoked AMPA-EPSCs in the absence (left) and presence (right) of sperimine (1 mM) in the pipette solution. Data derived from different MNTB neurons in the same slice. Sample traces are evoked EPSCs in the presence of D-APV (50 mM) recorded at different holding potentials (-100mV to +60 mV, superimposed). The EPSC amplitude was normalized to that at –60 mV. The rectification index (+60 mV / -60 mV) in the presence of spermine was 0.3. The rectification index decreased to 0.12 at P21 (n = 4). Consistently the GluR2 immunoreactivity decreased by 50% from P7 to P21 (data not shown) despite no significant change in GluR2 transcript (Fig. 7A).
