Figure 4. NMDARs do not limit temporal encoding within the physiological range.

A, OFF Alpha cell spike responses, measured using loose-patch recording, to square-wave temporal contrast modulation from 1 to 18.7 Hz. These frequencies covered the physiological response range, with peak responsiveness near ∼9 Hz. In these recordings, synaptic inhibition was intact. Error bars indicate ±SEM across cells (with number of cells in parentheses above the data points). B, synaptic currents recorded from an OFF Alpha cell in response to 12.5 Hz square-wave modulation at two of eight V_holds (left); recordings were made with inhibition and the ON pathway suppressed (l-AP4, gabazine, strychnine), to isolate the excitatory input, and the response to one cycle was averaged over the final 2 s of the stimulus (as in Fig.3). For a response window near the peak of excitation (grey box), an I–V relationship is shown (right) with a basis-function fit (continuous line). The response depends strongly on an NMDAR-mediated conductance, as indicated by the J-shaped I–V relationship. C, fitted conductances for responses to 1–18.7 Hz contrast modulation. Error bars indicate ±SEM across cells (with number of cells in parentheses above the data points). NMDAR-mediated conductances were scaled to their value at V_M = −62 mV, reflecting 8.1% of the maximal conductance (Manookin et al. 2010). The shape of the temporal tuning function does not match the function for spikes, in A, probably due to the effect of inhibition shaping the response under control conditions (A).