. It is commonly held that hearing generally begins on incubation day 12 (E12) in the chicken embryo (Gallus domesticus). However, little is known about the response properties of cochlear ganglion neurons for ages younger than E18. We studied ganglion neurons innervating the basilar papilla of embryos (E12-E18) and hatchlings (P13-P15). We asked first, when do primary afferent neurons begin to encode sounds? Second, when do afferents evidence frequency selectivity? Third, what range of characteristic frequencies (CFs) is represented in the late embryo? Finally, how does sound transfer from air to the cochlea affect responses in the embryo and hatchling? Responses to airborne sound were compared with responses to direct columella footplate stimulation of the cochlea. Cochlear ganglion neurons exhibited a profound insensitivity to sound from E12 to E16 (stages 39 -42). Responses to sound and frequency selectivity emerged at about E15. Frequency selectivity matured rapidly from E16 to E18 (stages 42 and 44) to reflect a mature range of CFs (170 -4,478 Hz) and response sensitivity to footplate stimulation. Limited high-frequency sound transfer from air to the cochlea restricted the response to airborne sound in the late embryo. Two periods of ontogeny are proposed. First is a prehearing period (roughly E12-E16) of endogenous cochlear signaling that provides neurotrophic support and guides normal developmental refinements in central binaural processing pathways followed by a period (roughly E16 -E19) wherein the cochlea begins to detect and encode sound.

This study examined the nature of spontaneous discharge patterns in cochlear ganglion cells in embryonic day 13 (E13) to early E17 chicken embryos (stages 39-43). Neural recordings were made with glass micropipettes. No sound-driven activity was seen for the youngest embryos (maximum intensity 107 dB sound pressure level). Ganglion cells were labeled with biotinylated dextran amine in four embryos. In two animals, primary afferents projected to hair cells in the middle region along the length of the basilar papilla in which, in one cell, the terminals occupied a neural transverse position and, in the other, a more abneural location. Statoacoustic ganglion cells showing no spontaneous activity were seen for the first time in the chicken. The proportion of "silent" cells was largest at the youngest stages (stage 39, 67%). In active cells, mean spontaneous discharge rates [9.4 +/- 10.4 spikes (Sp)/sec; n = 44] were lower than rates for older embryos (19 +/- 17 Sp/sec) (Jones and Jones, 2000). Embryos at stages 39-41 evidenced even lower rates (4.2 +/- 5.0 Sp/sec). The most salient feature of spontaneous activity for stages 39-43 was a bursting discharge pattern in >75% of active neurons (33 of 44). Moreover, in 55% of these cells, there was a clear, slow, rhythmic bursting pattern. The proportion of cells showing rhythmic bursting was greatest at the youngest stages (39-42) and decreased to <30% at stage 43. Rate of bursting ranged from 1 to 54 bursts per minute. The presence of rhythmic bursting in cochlear ganglion cells at E13-E17 provides an explanation for the existence of such patterns in central auditory relays. The bursting patterns may serve as a patterning signal for central synaptic refinements in the auditory system during development.

In the lamprey, spinal locomotor activity can be initiated by pharmacological microstimulation in several brain areas: rostrolateral rhombencephalon (RLR); dorsolateral mesencephalon (DLM); ventromedial diencephalon (VMD); and reticular nuclei. During DLM- or VMD-initiated locomotor activity in in vitro brain/spinal cord preparations, application of a solution that focally depressed neuronal activity in reticular nuclei often attenuated or abolished the locomotor rhythm. Electrical microstimulation in the DLM or VMD elicited synaptic responses in reticulospinal (RS) neurons, and close temporal stimulation in both areas evoked responses that summated and could elicit action potentials when neither input alone was sufficient. During RLR-initiated locomotor activity, focal application of a solution that depressed neuronal activity in the DLM or VMD abolished or attenuated the rhythm. These new results suggest that neurons in the RLR project rostrally to locomotor areas in the DLM and VMD. These latter areas then appear to project caudally to RS neurons, which probably integrate the synaptic inputs from both areas and activate the spinal locomotor networks. These pathways are likely to be important components of the brain neural networks for the initiation of locomotion and have parallels to locomotor command systems in higher vertebrates.

In larval lamprey, movements and muscle activity during swimming and burrowing behaviors were compared. Burrowing consisted of two components: an initial component in which the head was driven into the burrowing medium; and a final component in which the animal pulled the rest of its body into the burrowing medium. The initial component of burrowing was characterized by large undulatory movements and rhythmic muscle burst activity that were similar in form to those during fast swimming, but more intense. During the initial component of burrrowing, burst durations, burst amplitudes, and burst proportions of motor activity were larger than those during swimming, while cycle time was slightly shorter than during swimming. Intersegmental phase lags and right-left phase values were similar for swimming and initial burrowing. The final component of burrowing was characterized by sharp, long-duration flexures on one side of the body, sometimes followed by similar flexures on the other side. Each flexure was produced by long-duration, large-amplitude muscle burst activity on the same side of the body or several shorter sequential bursts with slightly smaller amplitudes. During the final component of burrowing, burst durations and burst amplitudes of motor activity were much larger than those during swimming or during the initial component of burrowing. It is suggested that the motor patterns for swimming and the initial component of burrowing are produced by a common spinal locomotor network. The final component of burrowing may use some of the same neurons in the spinal locomotor networks, but the networks are probably configured differently than the situation during swimming.

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