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The Journal of Neuroscience, September 15, 2002, 22(18):8101-8109

Extrasynaptic 7-Nicotinic Acetylcholine Receptor Expression in Developing Neurons Is Regulated by Inputs, Targets, and Activity

Craig L. Brumwell, James L. Johnson, and Michele H. Jacob

Department of Neuroscience, Tufts University, Sackler School of Biomedical Sciences, Boston, Massachusetts 02111

7-Nicotinic acetylcholine receptors (nAChRs) are widely expressed in the vertebrate nervous system. 7-nAChR functions include postsynaptic transmission, modulating neurotransmitter release, reinforcing nicotine addiction, and a role in neurological disorders, such as schizophrenia and Alzheimer's disease. In chick parasympathetic ciliary ganglion (CG) neurons, 7-nAChRs are excluded from the synapse and localize perisynaptically. Despite their extrasynaptic distribution, the highly Ca²⁺-permeable 7-nAChRs have important synapse-related Ca²⁺-dependent signaling functions in the CG. We show here that the synaptic partners regulate 7-nAChR expression during synapse formation in embryonic CG neurons in situ. The absence of inputs and target tissues cause reductions in 7-nAChR mRNA and protein levels that primarily resemble those seen for synaptic 3-nAChRs. However, there is a difference in their regulation. 7-nAChR levels are downregulated by reduced activity, whereas 3-nAChR levels are not. We propose that the activity-dependent regulation of extrasynaptic 7-nAChR levels may be an important mechanism for postsynaptic CG neurons to detect changes in presynaptic activity levels and respond with Ca²⁺-dependent plasticity changes in gene expression.

Key words: nicotinic acetylcholine receptor; nAChR; 7; 3; neuron-specific gene expression; synapse formation; innervation; target tissue interactions; induction; electrical activity; visual deprivation; ciliary ganglion; neuron

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22188101-09$05.00/0

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