Figure 6. Optogenetic Activation of MC Axons Reveals a Much Larger Excitatory Effect under Conditions Simulating SE Onset.

(A) Timeline.

(B) DrD2-Cre^+/− mice were injected with AAV2-DIO-hChR2(H134R)-eYFP in the left anterior or posterior hippocampus. Slices with MC axons distal to the injection site (ipsilateral or commissural; red dashes) were used to test the effects of brief light pulses on patched GCs.

(C) Representative viral expression of commissurally projecting MC axons located in the IML of the contralateral hemisphere (arrow). Scale bar: 200 μm.

(D1) Representative schematic of the DG. Note the MC axon terminating in the IML (red arrow).

(D2) 473 nm of light was aimed at the IML, the location of intense viral expression, while patching nearby GCs.

(E1) A brief pulse of light (2 ms; blue arrow) produced a weak depolarization under baseline conditions (black arrow).

(E2) After pharmacological simulation of SE began, the depolarization evoked by light became larger and prolonged (black arrow).

(E3) Within 25 min of simulating SE, the same light pulse triggered a paroxysmal depolarizing shift in the GC (PDS; black arrow).

(F) The intrinsic properties of the cell in (E) identified it as a GC (Scharfman, 1992, 1995a), including a triphasic afterhyperpolarization potential (F1) and current pulses that evoked responses with a short time constant and linear I-V relationship (F2 and F3).

See also Figure S4.