molecular layer · extracellular / voltage-clamp teaching model
Readout
Both windows track the same underlying change in synaptic strength; this switches units and the sample trace shape only.
Induction protocol
−20 mV
−70 mV (rest)0 mV
Sets granule-cell depolarization directly, decoupled from the presynaptic pattern above, so you can probe NMDAR coincidence detection on its own — before feedforward inhibition is subtracted from it.
Feedforward inhibition (GABAA)
65%
0% (disinhibited)100% (max shunt)
Perforant-path pulses drive feedforward interneurons disynaptically, shunting granule-cell depolarization before it can relieve the NMDAR Mg²⁺ block. This is why LTP here is harder to obtain than at Schaffer collateral→CA1.
Run
NMDAR coincidence detection vs. feedforward shunt
Mg²⁺ block relieved—
GABAA shunt (train 1)—
NMDAR Ca²⁺ influx (last induction)—
Time course — % baseline response
t = simulated recording time (min)fEPSP slope, mV/ms
Sample trace
baselinecurrentstimulus
inward current
t (min)
% baseline
fEPSP slope (mV/ms)
Session status
Protocol run
none yet
APV present
no
GABAA strength
65% (intact)
Holding potential
−20 mV
Current response
100 %
Trials (this protocol)
—
Run a baseline, choose a protocol, then induce LTP.