Figure 5. The extent of motor impairment showed little or no correlation with the C2-evoked VSI spiking recorded before blocking PdN6.

(A) A schematic illustration showing the stimulus (C2) and recording (VSI) microelectrodes, the direction of action potential propagation (dashed arrows) in C2 and VSI, and synaptic action (+, excitatory; −, inhibitory) of C2 onto VSI before blocking PdN6. Repetitive square current pulses (10 nA, 20 ms) were injected into the C2 soma to evoke a train of action potentials at a constant frequency (10 Hz). (B) Two examples of swim motor patterns (Bi, Bii) and the membrane potential responses (Biii, Biv) of VSI to C2 stimulation are shown for two animals (Animals 3 and 4). With PdN6 intact, Animal 3 showed five VSI bursts (Bi) and Animal 4 had six VSI bursts (Bii). The effect of C2 stimulation on VSI varied among individuals; causing an intense burst in VSI of Animal 3 (Biii) but only two spikes in Animal 4 (Biv). VSI exhibited antidromic spikes in the majority of preparations (see text) that were presumably caused by the C2 excitatory action in the distal terminal of VSI (Sakurai and Katz, 2009b). In Biii and Biv action potentials are truncated to show underlying membrane potential. (C) No correlation was detected between the number of VSI bursts per swim episode and the number of C2-evoked VSI spikes with PdN6 intact (R² = 0.05, p = 0.10 by linear regression, N = 52). Graph symbols in this and Figures 6 and 7 each represent data from the same individuals.

DOI: http://dx.doi.org/10.7554/eLife.02598.009