RT Journal Article
SR Electronic
T1 Extrasynaptic α7-Nicotinic Acetylcholine Receptor Expression in Developing Neurons Is Regulated by Inputs, Targets, and Activity
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 8101
OP 8109
DO 10.1523/JNEUROSCI.22-18-08101.2002
VO 22
IS 18
A1 Craig L. Brumwell
A1 James L. Johnson
A1 Michele H. Jacob
YR 2002
UL http://www.jneurosci.org/content/22/18/8101.abstract
AB α7-Nicotinic acetylcholine receptors (nAChRs) are widely expressed in the vertebrate nervous system. α7-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, α7-nAChRs are excluded from the synapse and localize perisynaptically. Despite their extrasynaptic distribution, the highly Ca2+-permeable α7-nAChRs have important synapse-related Ca2+-dependent signaling functions in the CG. We show here that the synaptic partners regulate α7-nAChR expression during synapse formation in embryonic CG neurons in situ. The absence of inputs and target tissues cause reductions in α7-nAChR mRNA and protein levels that primarily resemble those seen for synaptic α3-nAChRs. However, there is a difference in their regulation. α7-nAChR levels are downregulated by reduced activity, whereas α3-nAChR levels are not. We propose that the activity-dependent regulation of extrasynaptic α7-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.