PT  - JOURNAL ARTICLE
AU  - Craig L. Brumwell
AU  - James L. Johnson
AU  - Michele H. Jacob
TI  - Extrasynaptic α7-Nicotinic Acetylcholine Receptor Expression in Developing Neurons Is Regulated by Inputs, Targets, and Activity
AID  - 10.1523/JNEUROSCI.22-18-08101.2002
DP  - 2002 Sep 15
TA  - The Journal of Neuroscience
PG  - 8101--8109
VI  - 22
IP  - 18
4099  - http://www.jneurosci.org/content/22/18/8101.short
4100  - http://www.jneurosci.org/content/22/18/8101.full
SO  - J. Neurosci.2002 Sep 15; 22
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.