Figure 9.

Schematic drawing of pathways possibly contributing to patterning and phasing of fMN activity in one segment of the caudal lamprey spinal cord. For better clarity network topology is presented without distinction between local and intersegmental projections. The excitatory CPG kernel driving mMNs on either side of the spinal cord is depicted as a box. These burst generating kernels are active in antiphase by way of interposed mutually inhibiting interneurons (Cangiano and Grillner, 2003, 2005) [inhibitory contralaterally and caudally projecting interneurons (CC-I)]. The excitatory kernels drive not only ipsilateral mMNs, but also more weakly fMNs. The connection to the fMNs is dashed because this influence is only detected after 50–70% lesioning of the spinal cord midline as well as in the hemi cord. The specific connection of excitatory CC-E interneurons with fMNs, presented in this study, seems to be monosynaptic. A potential neural source for the in-phasic inhibitory drive that fMNs receive during fictive locomotion is given (stippled iINs). Gray neurons and/or connections have been described previously; black neurons and/or connections are newly identified; stippled neurons and/or connections are hypothetical.