The effect of lesions in the neural crest on the formation of synaptic connexions in the embryonic chick spinal cord

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Abstract
The pattern of synaptic activity in lateral gastrocnemius (lg) motoneurons in the lumbar spinal cord of chick embryos (stage 44-45, 19-21 d [day] of incubation) was examined using intracellular recording. In the motoneurons of normal chick embryos, stimulation of different peripheral, sciatic nerve branches gave rise to characteristic synaptic responses. Stimulation of the lateral gastrocnemius nerve caused a monosynaptic EPSP [excitatory post-synaptic potential] which was graded by the intensity of nerve stimulation. Stimulation of synergistic muscle afferents also caused a brief latency EPSP, followed by longer latency excitatory and inhibitory synaptic potentials. Stimulation of antagonistic muscle afferents or cutaneous afferents gave rise to longer latency inhibitory and excitatory synaptic potentials, respectively. The synaptic activity of lg motoneurons was also recorded in embryos in which short segments of the lumbar neural crest had been destroyed by microcautery at 3 d of incubation (stage 18). The embryos developed without sensory ganglia and dorsal roots in the corresponding region. At 19-21 d of incubation, the amplitude of lg EPSP lg motoneurons in deafferented segments was, on average, only 1/2-1/3 of the amplitude in motoneurons of intact spinal segments. Both the lg and synergist EPSP were larger than those in acutely deafferented segments of normal embryos. Despite the weak monosynaptic input from lg and synergistic afferents, the pattern of synaptic activity evoked by antagonistic muscle afferent or cutaneous afferent stimulation was not different then normal. This was even the case for gastrocnemius motoneurons in which no early EPSP could be evoked by stimulating the lg or synergistic muscle nerves. No muscle spindles could be seen in sections of lg muscles from embryos with extensive lesions of the lumbosacral neural crest. Incomplete lesions of lg segments reduced the number of spindles in the muscle. Apparently, when motoneurons are deprived of part of their normal synaptic input before the formation of peripheral connections, the identity of the motoneurons (in terms of the origin of their synaptic input) is preserved. Missing synaptic inputs are either replaced by appropriate afferent fibers, if they are available, or not replaced. Chick sensory ganglion cells with monosynaptic connections to motoneurons appear to be unable to compensate significantly for peripheral or central defects in the innervation of the hind limb. They behave as if their developmental possibilities were quite rigidly determined at an early embryonic stage.