Figure 3.

Subcellular mechanisms of GrC and GoC responses. Response of two exemplar GrCs and one GoC activated by a mf burst (five spikes at 500 Hz on eight contiguous mfs). The top traces show intracellular membrane potential while the bottom traces show the synaptic membrane currents. All glutamate receptor-dependent currents (A = AMPA, N = NMDA, K = kainate) are downward while the GABA-A receptor-mediated currents (G = GABA-A: α1 and α6 receptor-mediated currents together) are upward, except when changes in the driving force invert the current sign (glutamate reversal potential = 0 mV and GABA reversal potential = −65 mV). GrC₁ receives only 1 mf input, GrC₂ receives 3 mf inputs and 2 GoC inputs. Note inhibition of spike generation by evoked IPSCs in GrC₂ (arrow). In contrast to AMPA current short-term depression, the inset shows the NMDA and GABA-A currents build-up up on enlarged scale (vertical axis ×5). In GoCs, several pf and mf synapses contribute to generate the glutamatergic inputs on apical and basal dendrites, respectively. The pf input involves activation of AMPA, NMDA and kainate receptors, while the mf input activates AMPA and NMDA receptors. The inhibitory input from molecular layer interneurons (MLI) occurs on the apical dendrites. Note generation of a spike doublet by the EPSCs occurring through the feed-forward (filled arrow) and feed-back (open arrow) loops. The pf EPSCs occur with some delay compared to mf EPSCs, accounting for the time required for GrC excitation and pf-GrC transmission, and are interrupted by GoC inhibition of GrCs. MLIs intensify their action just after GrC discharge contributing to terminate GoC inhibition on GrCs.