Spontaneous embryonic movements, called embryonic motility, are produced by correlated spontaneous activity in the cranial and spinal nerves, which is driven by brainstem and spinal networks. Using optical imaging with a voltage-sensitive dye, we have revealed previously that this correlated activity is a widely propagating wave of neural depolarization, which we termed the depolarization wave. We have observed in the chick and rat embryos that the activity spread over an extensive region of the central nervous system, including the spinal cord, hindbrain, cerebellum, midbrain, and forebrain. One important consideration is whether a depolarization wave with similar characteristics occurs in other species, especially in different mammals. Here, we provide evidence for the existence of the depolarization wave in the mouse embryo by showing that the widely propagating wave appeared independently of the localized spontaneous activity detected previously with Ca2+ imaging. Pregnant mice were anesthetized with ether, and the spinal cord was dislocated at the cervical level. Their fetuses were then surgically removed, and the whole brain-spinal cord or brainstem-spinal cord preparation was dissected in an ice-cold solution. We mapped the origin of the depolarization wave and revealed that the wave generator moved from the rostral spinal cord to the caudal cord as development proceeded, and was later replaced with mature rhythmogenerators. Furthermore, we examined the pharmacological nature of the mouse depolarization wave and its developmental changes. We show here that two types of switching in pharmacological characteristics occur during development. One is that the depolarization wave is strongly dependent on nicotinic acetylcholine receptors during the early developmental stage (E11-E12), but is dominated by glutamate at the later stage (E13~). The second is that GABA, which acts as an excitatory mediator of the depolarization wave during the early phase, becomes an inhibitory modulator by E14. These changes seemed to occur earlier in the hindbrain than in the spinal cord. We also show that the second switching causes the loss of synchronization over the network, resulting in the disappearance of the depolarization wave and a segregation of the activity into discrete regions of the medulla and spinal cord. The present study shows that a synchronized wave with common characteristics is expressed in different species, suggesting fundamental roles in neural development.