Journal of Neuroscience, Vol 13, 4525-4537, Copyright © 1993 by Society for Neuroscience
Reduced levels of acetylcholine receptor expression in chick ciliary ganglion neurons developing in the absence of innervation
LS Arenella, JM Oliva and MH Jacob
Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545.
Chick ciliary ganglion neurons receive innervation from a single source,
the accessory oculomotor nucleus (AON), and nicotinic ACh receptors (AChRs)
mediate chemical synaptic transmission through the ganglion. Previous
experiments examining the developmental expression of AChRs in embryonic
chick ciliary ganglion neurons in situ have shown that AChR levels increase
substantially in the neurons at the time of innervation. Prior to synapse
formation, few AChRs are detected in the neurons. In the present
experiments, the role of presynaptic inputs in inducing an increase in
AChRs was established by examining AChR levels in ciliary ganglion neurons
that have been deprived of innervation by surgical ablation of the AON
prior to synapse formation. AChR levels were dramatically reduced in
neurons of input-deprived ganglia as compared to control innervated neurons
at all developmental stages examined from embryonic day (ED) 5 to ED 12 as
determined by indirect immunocytochemical labeling of frozen ganglion
sections with the anti- AChR monoclonal antibody mAb 35, and light
microscopy. In contrast, neuronal somata of input-deprived and control
ganglia had equivalent levels of immunolabeling for three other components,
a transmembrane glycoprotein of synaptic vesicles, SV2, and two
microtubule-associated proteins, MAP 1B and MAP 2, from ED 5 up to ED 10.
The results demonstrate that presynaptic inputs specifically increase the
levels of AChR expression in developing neurons. In addition, changes in
the levels of immunolabeling for AChRs, SV2, MAP 1B, and MAP 2 in neuronal
somata after ED 10 demonstrate that other major developmental events also
influence the levels of these components in neurons. Declines in the
intensity of AChR, SV2, MAP 1B, and MAP 2 immunolabeling within a subset of
neuronal somata in both operated and control ganglia at ED 10 and 12
coincide with the period of neuronal cell death. Increases in AChR labeling
in the rest of the neuronal population of input-deprived ganglia at ED 12
suggest that, in addition to innervation, synapse formation with the
peripheral target tissue influences AChR levels in developing neurons in
situ.
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