Figure 5. Cholinergic excitation shapes temporal E/I temporal offsets under physiological conditions.

(A) The EPSCs and IPSCs elicited in a DSGC for preferred and null stimuli, in control (black), and in the presence of a nicotinic acetylcholine receptor antagonist (hexamethonium, HEX; red traces). A normalized version of the EPSC measured in HEX (light red trace) is illustrated to emphasize the delay in excitation that occurs when cholinergic receptors are blocked. (B) The directional tuning of the E/I temporal offsets in control and HEX averaged across 8 cells. The offsets were aligned to the preferred direction (P) of the spike responses, which were measured in the same DSGC before performing the whole cell recording. HEX significantly reduced the E/I temporal offsets across all directions (p<0.01). Data are represented as mean ± SEM. (C) The directional tuning of the timing delay of the EPSC in HEX relative to control (n = 8). Data are represented as mean ± SEM. The increased onset latency observed in HEX continued to be observed when inhibition was blocked, indicating that they cannot be accounted for by large voltage–clamp errors associated with inhibitory conductances (Figure 5—figure supplement 1).

Figure 5—figure supplement 1. The EPSC timing delay in HEX is independent of inhibition.

(A – B) The EPSCs elicited in a DSGC to preferred (A) and null stimuli (B), in control, HEX (to block nicotinic acetylcholine receptors), and HEX + SR-95531 (to block GABA_A receptors). Note that the responses have been normalized to show that the timing of the EPSCs is altered upon addition of HEX, but not upon further addition of SR. (stimulus velocity = 600 μm/s) (C–D) The onset of the preferred (C) and null EPSCs (D) in control (n = 10), HEX (n = 10), and HEX +SR (n = 7) shown relative to HEX. The EPSCs in HEX were significantly delayed to control (*p<0.001). But further addition of SR did not alter the timing. Pooled data are represented as mean ± SEM.