Models #1a,1b: Compound EPSPs, IPSP-controlled burst offset
In order to more closely fit the voltage behavior of the model to experimental data, the maximum conductance values of each channel type and the decay time of respective EOCD and primary afferent EPSP inputs to the granular cell were allowed to vary. A GABAergic IPSP (t decay=15ms, reversal potential= -65mV, maximum conductance = 0.005m S) was delivered to the granular cell at 57ms post-EOCD onset in order to limit the length of the burst to experimentally shown response duration in these cells. Although such a burst-ending role has not been experimentally shown for LMI cells in vivo, it seems plausible that accumulation of extracellular K+ in the cleft between the granular cell soma and the presynaptic LMI terminal during the burst could trigger GABA release via ephaptic depolarization (Han et al., 2000). A mechanism whereby GABA release was inhibited during the early part of the burst, possibly via unknown connections between the juxtalobar or afferent fibers and the LMI cell, would enable this IPSP to be relatively time-locked to the onset of EOCD or primary afferent inputs.