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The Journal of Neuroscience, September 14, 2005, 25(37):8555-8566; doi:10.1523/JNEUROSCI.1983-05.2005

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Cellular/Molecular
A Null Mutation for the 3 Nicotinic Acetylcholine (ACh) Receptor Gene Abolishes Fast Synaptic Activity in Sympathetic Ganglia and Reveals That ACh Output from Developing Preganglionic Terminals Is Regulated in an Activity-Dependent Retrograde Manner

Siamak Rassadi,^1 * Arjun Krishnaswamy,^1 * Brigitte Pié,¹ Russell McConnell,² Michele H. Jacob,² and Ellis Cooper¹

¹Department of Physiology, McGill University, Montreal, Quebec, Canada H3G 1Y6, and ²Department of Neuroscience, Tufts University, Boston, Massachusetts 02155

In vertebrates, synaptic activity exerts an important influence on the formation of neural circuits, yet our understanding of its role in directing presynaptic and postsynaptic differentiation during synaptogenesis is incomplete. This study investigates how activity influences synaptic differentiation as synapses mature during early postnatal life. Specifically, we ask what happens to presynaptic terminals when synapses develop without functional postsynaptic receptors and without fast synaptic transmission.

To address this issue, we investigated cholinergic nicotinic synapses in sympathetic ganglia of mice with a null mutation for the 3 nicotinic ACh receptor gene. Disrupting the 3 gene completely eliminates fast excitatory synaptic potentials on postganglionic sympathetic neurons, establishing a crucial role for 3-containing postsynaptic receptors in synaptic transmission. Interestingly, the preganglionic nerve terminals form morphologically normal synapses with sympathetic neurons, and these synapses persist without activity in postnatal animals. Surprisingly, when stimulating the preganglionic nerve at physiological rates, we discovered a significant decrease in ACh output from the presynaptic terminals in these 3^–/– sympathetic ganglia. We show that this decrease in ACh output from the presynaptic terminals results, in part, from a lack of functional high-affinity choline transporters. We conclude the following: (1) fast synaptic transmission in mammalian SCG requires 3 expression; (2) in the absence of activity, the preganglionic nerve forms synapses that appear morphologically normal and persist for several weeks; and (3) to sustain transmitter release, developing presynaptic terminals require an activity-dependent retrograde signal.

Key words: nicotinic receptors; cholinergic synaptic transmission; high-affinity choline transporter; muscarinic receptors; autonomic nervous system; synapse formation

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Received May 17, 2005; revised July 28, 2005; accepted August 4, 2005.

This article has been cited by other articles:

				B. Lendvai and E. S. Vizi Nonsynaptic Chemical Transmission Through Nicotinic Acetylcholine Receptors Physiol Rev, April 1, 2008; 88(2): 333 - 349. [Abstract] [Full Text] [PDF]

				V. A. Campanucci, A. Krishnaswamy, and E. Cooper Mitochondrial Reactive Oxygen Species Inactivate Neuronal Nicotinic Acetylcholine Receptors and Induce Long-Term Depression of Fast Nicotinic Synaptic Transmission J. Neurosci., February 13, 2008; 28(7): 1733 - 1744. [Abstract] [Full Text] [PDF]

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