Figure 7.

Presynaptic somatic membrane potential modulates synaptic transmission via the slow inactivation of axonal Kv1 channels in neocortical pyramidal cells. A, Recording protocol from Shu and others (2006) in which the presynaptic layer 5 pyramidal cell membrane potential is alternatively held near rest (−62 mV in this example) or near firing threshold (−48 mV), and brief stimuli produce action potentials (APs; at 0.8 Hz) from each membrane potential. The resulting excitatory post-synaptic potential (EPSPs) in the postsynaptic pyramidal cell are shown in B. B, APs produce facilitated postsynaptic responses when the presynaptic membrane is depolarized (−48 mV; red trace). C, Average time course of facilitation and disfacilitation of EPSPs. Adapted by permission from Macmillan Publishers Ltd: Nature (Shu and others 2006), © 2006. D, Depolarized presynaptic membrane potential-induced facilitation of EPSPs is abolished by Kv1 channel blocker dendrotoxin-I (DTX-I). Plot illustrates the facilitation of EPSPs by increasing durations (Δt) of presynaptic depolarization (solid circles) and block by DTX-I (open circles). Modified from Kole and others (2007) with permission from Elsevier. E, F, Somatic depolarization and DTX-I do not increase unitary AP-evoked GABA postsynaptic potentials (uGPSP) in fast-spiking (FS) interneuron → pyramidal cell (PC) pairs. E, APs evoked from depolarized presynaptic potentials (green traces; −50 mV; sufficient to produce Kv1 channel inactivation based on lack of delayed firing in presynaptic FS cell, E₁) or hyperpolarized (~−70 mV) potentials (black traces) produce no change in uGPSP amplitude. However, application of 1 mM TEA, which blocks Kv3 channels, produces an approximately twofold increase in uGPSP amplitude, consistent with previous results (Goldberg and others 2005). F, Bath application of DTX-I has no effect on uGPSP amplitude in FS → PC pairs. F₁, Summary data (n = 3). Modified from Goldberg and others (2008) with permission from Elsevier.