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The Journal of Neuroscience, October 12, 2005, 25(41):9347-9357; doi:10.1523/JNEUROSCI.1800-05.2005

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Development/Plasticity/Repair
Disruption and Recovery of Patterned Retinal Activity in the Absence of Acetylcholine

Rebecca C. Stacy,^1 * Jay Demas,^1 * Robert W. Burgess,^1,2 Joshua R. Sanes,^1,3 and Rachel O. L. Wong¹

¹Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, ²The Jackson Laboratory, Bar Harbor, Maine 04609, and ³Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138

Many developing neural circuits generate synchronized bursting activity among neighboring neurons, a pattern thought to be important for sculpting precise neural connectivity. Network output remains relatively constant as the cellular and synaptic components of these immature circuits change during development, suggesting the presence of homeostatic mechanisms. In the retina, spontaneous waves of activity are present even before chemical synapse formation, needing gap junctions to propagate. However, as synaptogenesis proceeds, retinal waves become dependent on cholinergic neurotransmission, no longer requiring gap junctions. Later still in development, waves are driven by glutamatergic rather than cholinergic synapses. Here, we asked how retinal activity evolves in the absence of cholinergic transmission by using a conditional mutant in which the gene encoding choline acetyltransferase (ChAT), the sole synthetic enzyme for acetylcholine (ACh), was deleted from large retinal regions. ChAT-negative regions lacked retinal waves for the first few days after birth, but by postnatal day 5 (P5), ACh-independent waves propagated across these regions. Pharmacological analysis of the waves in ChAT knock-out regions revealed a requirement for gap junctions but not glutamate, suggesting that patterned activity may have emerged via restoration of previous gap-junctional networks. Similarly, in P5 wild-type retinas, spontaneous activity recovered after a few hours in nicotinic receptor antagonists, often as local patches of coactive cells but not waves. The rapid recovery of rhythmic spontaneous activity in the presence of cholinergic antagonists and the eventual emergence of waves in ChAT knock-out regions suggest that homeostatic mechanisms regulate retinal output during development.

Key words: retina; wave; homeostasis; acetylcholine; gap junction; development

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Received May 4, 2005; revised August 28, 2005; accepted August 29, 2005.

This article has been cited by other articles:

				J. E. Cook and D. L. Becker Gap-Junction Proteins in Retinal Development: New Roles for the "Nexus" Physiology, August 1, 2009; 24(4): 219 - 230. [Abstract] [Full Text] [PDF]

				J. L. Lefebvre, Y. Zhang, M. Meister, X. Wang, and J. R. Sanes {gamma}-Protocadherins regulate neuronal survival but are dispensable for circuit formation in retina Development, December 15, 2008; 135(24): 4141 - 4151. [Abstract] [Full Text] [PDF]

				C. Sun, D. K. Warland, J. M. Ballesteros, D. van der List, and L. M. Chalupa Retinal waves in mice lacking the {beta}2 subunit of the nicotinic acetylcholine receptor PNAS, September 9, 2008; 105(36): 13638 - 13643. [Abstract] [Full Text] [PDF]

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