PMC

Simulation design. (a) Three-compartment model with soma, axon hillock, and axon initial segment. Stimulation current was applied to the soma compartment and recordings were made in the soma and axon initial segment. (b) Ramps of current injected at the soma controlled the dVm/dt prior to a spike. Spikes were initiated in the axon initial segment and back-propagated to the soma. (c) The voltage threshold for spiking was determined empirically. All spikes shown are from the axon compartment. Left. Examples of spikes caused by supra-threshold stimulation (solid blue), spike failures caused by sub-threshold stimulation (dashed blue), and a spike caused by depolarization within 0.1 mV of threshold (solid black). Right. Close-up of spikes and spike failures. The bottom right shows that spike threshold (indicated by black square) was determined within 0.1 mV of sub-threshold (noted by bracket and arrow) and supra-threshold Vm values. Note that at the time of current ramp off-set, all Vm trajectories are determined by intrinsic membrane currents

Aa, elevation or reduction of arterial blood pressure (AP, mmHg) using aortic occlusion (AOc) or sodium nitroprusside (SNP) does not alter the discharge rate of this neurone. Ab, hypothalamic stimulation (arrow) applied outside the critical period after occurrence of a spontaneous spike (s) elicits an antidromic spike (a, top four traces) which frequently fails to invade the soma (IS in the second and fourth traces from top). Hypothalamic stimulation applied within the critical period after the spontaneous spike fails to elicit an antidromic spike (bottom three traces). Ac, left column, spontaneous spike (s), antidromic spike (a) and initial segment of antidromic spike (IS). Ac, right column, superposition of spontaneous and antidromic spike (top) and superposition of antidromic spike and antidromic initial segment (bottom). Ba, toe pinch elicits small increases in arterial blood pressure but fails to alter unit discharge consistently. Bb, cardiopulmonary receptor stimulation with phenylbiguanide (PBG, 10 μg kg⁻¹, i.v.) has no consistent effect on discharge rate.

Changing pNa_max⁺ in the soma and initial segment dramatically affects spike invasion into the soma. A stimulus pulse pair was applied to the 20th peripheral node (IPI, 2.26 ms) and recordings were made near the t-junction (R2 and R3 in ) and in the soma (R4 in ). The first stimulus pulse is marked with an arrow in bottom trace. The ability of the spike to invade the soma (R4) is compromised as pNa_max⁺ is reduced. At intermediate values of pNa_max⁺ the first spike invaded the soma, but the second spike failed to invade. At lower values, even the first spike failed to invade. Arrowheads in traces R2 and R3 indicate a decremental signal, originating in the soma spike, that is still visible at these recording points near the t-junction. This signal is subthreshold for spike propagation, however, and was not recorded at R1 or R5 (, data not shown). Note that using other parameters, the soma spike can generate a back-propagating “extra spike” as shown in . pNa_max⁺ values are: low, 4 × 10⁻⁵ cm/s; medium, 8 × 10⁻⁵ cm/s; high, 24 × 10⁻⁵ cm/s.

Distribution of latencies between subtracted EPSP waveform peaks and LGN spikes. A, For the cell in B, the time of the peaks in the subtracted waveforms are plotted, in order of latency, with respect to the peak of the axon initial segment potential. The axon initial segment potential was designated t = 0 because the somatodendritic spike often failed in this cell. The gap in the distribution near −1.5 ms is attributable to the refractory period of the EPSP. B, Distribution of latencies plotted for the cell in C. The latencies are shifted in this cell because they are plotted with respect to the peak of the somatodendritic potentials, which have a longer delay after EPSPs than the axon initial segment potentials. Parvo, Parvocellular; Magno, magnocellular.