Article Figures & Data
Figures
- Figure 1.
NMDA receptor subunit composition changes during early postnatal development. A, Responses to puffed NMDA (left) in a P7 Drd4 ganglion cell at a series of Vholds. The response, averaged within the rectangle, generated a J-shaped I–V plot (middle) that was reduced (right) in the presence of ifenprodil (10 μm). B, Ratio of the current measured at Vhold near +40 mV (INMDA +40 mV) in the presence of ifenprodil relative to the control condition. Numbers of cells for each point are shown in parentheses. Error bars indicate ±SEM. Ratios significantly less than one are indicated (*p < 0.01, **p < 0.001). C1, Ifenprodil reversibly attenuated the NMDA puff response in a P7 Drd4 cell (left; Vhold = +55 mV). C2, Ifenprodil reversibly attenuated INMDA +40 mV in a population of P7 and P14 Drd4 and TRHR cells.
- Figure 2.
Light-evoked responses are dominated by inhibition. A1, A P14 Drd4 ganglion cell response to 1 s of UV light (365 nm, 2 mm diameter). Here and elsewhere, synaptic currents are shown at the two indicated Vholds (in mV; left) and current responses averaged within the white (light-ON) and gray (light-OFF) rectangles are plotted versus Vhold (right). I–V plots were linear and reversed near ECl (−67 mV). A2, Averaged I–V plots for ON and OFF responses for a combined population of Drd4 and TRHR cells at P14 and P28. Error bars indicate ±SEM. B1, Same format as A1 in the presence of hexamethonium (100 μm) and gabazine (20 μm). I–V plot was J-shaped and reversed near Ecation (0 mV). B2, Population averages for the response in B1. C, Population averages when D-AP5 (100 μm) was added to hexamethonium and gabazine, blocking the J-shaped I–V relationship. D, Population averages when L-AP4 (50 μm) was added to hexamethonium and gabazine, blocking the ON response selectively.
- Figure 3.
NMDARs are activated by light-evoked glutamate release at P14 and P28 in both Drd4 and TRHR cells. A, Light-evoked responses in the presence of nicotinic and GABAA receptor block were fit (line) by the weighted sum of three basis functions: AMPAR, NMDAR, and inhibitory (GABA/glycine) receptors. B, Population fit of Drd4 light-onset response (left; as in Fig. 2A) and NMDA puff-evoked response (right; as in Fig. 1A) determined the GABA/Glycine and NMDA receptor basis functions. C, Synaptic currents and I–V plots from a P14 TRHR cell in response to 1 s of UV light (2 mm diameter) in the presence of hexamethonium (100 μm) and gabazine (20 μm). D, Same format as C in the presence of curare (50 μm) and gabazine (20 μm). The cell was targeted using two-photon imaging, and the stimulus was a 100% contrast-reversing spot (0.17 mm diameter) with a background at the mean luminance. E1, I–V plots from P14 Drd4 and TRHR cells were fit with basis functions (smooth curves in C, D) to determine the underlying ligand-gated conductances. ON and OFF responses showed significant AMPAR- and NMDAR-mediated conductances (gAMPA; gNMDA) at high (left) and low-intensites (right). Error bars indicate ±SEM. E2, Same as in E1 for 100% contrast square-wave stimuli. F–H, Same format as C–E for P28 cells, with a Drd4 example cell (F, G).
- Figure 4.
NMDARs activated by light-evoked glutamate release contain GluN2B subunits at P14 but show cell-type differences at P28. A, Synaptic currents and I–V plots in a P14 Drd4 cell in response to 1 s of UV light (2 mm diameter) in the presence of hexamethonium (100 μm) and gabazine (20 μm; left). Adding ifenprodil (10 μm, right) reduced the response. B, Conductance analysis of P14 Drd4 cells in the absence and presence of ifenprodil (10 μm) and the ratio of the conductance in ifenprodil relative to control (gifen/gcontrol). Error bars indicate ±SEM. C, Same format as in B for P14 TRHR cells. D–F, Same format as A–C. At P28, TRHR cells (F1) but not Drd4 cells (E), showed persisting sensitivity to ifenprodil, and this effect on TRHR cells continued at P35 (F2).
