Figure 7.

An updated model of the vocal CPG. A, Our results support the hypothesis that motor neuron collaterals form a cholinergic synapse onto interneurons in the motor nucleus that project to the premotor nucleus. These are likely inhibitory neurons and are hypothesized to synapse directly onto FTNs in DTAM. B, According to our model, inactivating motor neurons eliminates the feedback inhibition pathway (indicated by dashed lines). C, Hypothetical membrane potentials of FTNs in which the feedback signal is intact (black line) or disrupted (gray line). In the intact circuit, FTN spikes are following by IPSPs (shaded area). In the absence of the feedback signal (via transection, motor neuron silencing, or cholinergic antagonist), IPSPs no longer follow spikes, inducing increased firing rates. D, Hypothetical membrane potentials of three FTNs in an intact brain. In this scenario, spike synchrony is ensured by motor neuron-dependent IPSPs, leading to entrained patterns of postinhibitory rebound. E, Membrane potentials of three hypothetical FTNs in which feedback inhibition is eliminated. When FTNs no longer receive simultaneous IPSPs, spikes are no longer entrained, and each cell generates a faster spike train without temporal coordination between neurons.