Transient GABA immunoreactivity in cranial nerves of the chick embryo

Authors

  • Christopher S. von Bartheld,

    1. Hearing Development Laboratories, University of Washington, Seattle, Washington 98195
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  • Edwin W. Rubel

    Corresponding author
    1. Hearing Development Laboratories, University of Washington, Seattle, Washington 98195
    • Hearing Development Laboratories, RL-30, University of Washington, Seattle, WA 98195
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Abstract

The distribution and time course of γ-aminobutyric acid (GABA) immunoreactivity was investigated in the cranium of the chick embryo from 2 to 16 days of incubation (E2–16). A fraction of nerve fibers transiently stains GABA-positive in all cranial motor nerves and in the vestibular nerve. Cranial motor nerves stain GABA-positive from E4 to E11, including neuromuscular junctions at E8–11; labeled fibers are most frequent in the motor trigeminal root (E6–9.5). Substantial GABA staining is present from E4 to E10 in a subpopulation (1–2%) of vestibular ganglion cells. Their peripheral processes are labeled in the vestibular endorgan, predominantly in the posterior crista. Some GABA-positive fibers are present in the olfactory nerve (after E5) and in the optic nerve (after E9.5); their immunoreactivity persists throughout the period investigated. Transient GABA immunoreactivity follows “pioneer” fiber outgrowth and coincides with the formation of early synaptic contacts.

GABA-containing neurons may change their neuronal phenotype (loss of GABA expression) or they may be eliminated by embryological cell death. Periods of cell death were determined in cranial ganglia and motor nuclei by aggregations of pycnotic cells in the same embryonic material. The periods of embryonic cell death partly coincide with transient GABA immunoreactivity. The function(s) of transient GABA expression is unknown. Some lines of evidence suggest that GABA has neurotrophic functions in developing cranial nerves or their target tissue. In the developing neuromuscular junction, GABA may be involved in the regulation of acetylcholine receptors.

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