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The Journal of Neuroscience, December 12, 2007, 27(50):13581-13589; doi:10.1523/JNEUROSCI.3863-07.2007
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Development/Plasticity/Repair
Synaptic Reorganization in Scaled Networks of Controlled Size
Nathan R. Wilson,1 * Michael T. Ty,2 * Donald E. Ingber,2 Mriganka Sur,1 andGuosong Liu1,3 1Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, 2Department of Pathology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, and 3Center for Learning and Memory, School of Medicine, Tsinghua University, Beijing 100084, China
Correspondence should be addressed to either of the following: Dr. Nathan R. Wilson, Massachusetts Institute of Technology, 46-6227, 77 Massachusetts Avenue, Cambridge, MA 02139, Email: nathan1{at}mit.edu; or Dr. Guosong Liu, School of Medicine, Tsinghua University, Beijing 100084, China, E-mail: Email: liu.guosong{at}gmail.com
Neurons in plastic regions of the brain undergo fundamental changes in the number of cells connecting to them as a result of development, plasticity and disease. Across these same time periods, functional changes in cellular and synaptic physiology are known to occur and are often characterized as developmental features of these periods. However, it remains possible that many such changes are direct consequences of the modified degree of partnering, and that neurons intrinsically scale their physiological parameters with network size. To systematically vary a recurrent network's number of neurons while measuring its synaptic properties, we used microfabricated extracellular matrix adhesive islands created with soft lithography to culture neuronal clusters of precise sizes, and assessed their intrinsic connectivity using intracellular recordings and confocal microscopy. Both large and small clusters supported constant densities of excitatory and inhibitory neurons. However, neurons that were provided with more potential partners (larger clusters) formed more connections per cell via an expanded dendritic surface than cocultured smaller clusters. Electrophysiologically, firing rate was preserved across clusters even as size and synapse number increased, due in part to synapses in larger networks having reduced unitary strengths, and sparser paired connectivity. Larger networks also featured a particular increase in the number of excitatory connections onto inhibitory dendrites. We suggest that these specific homeostatic mechanisms, which match the number, strength, and architecture of connections to the number of total available cellular partners in the network, could account for several known phenomena implicated in the formation, organization and degeneration of neuronal circuits.
Key words: synapse; network; inverse; quantal; homeostasis; inhibition
Received Aug. 24, 2007; revised Oct. 18, 2007; accepted Oct. 22, 2007.
Correspondence should be addressed to either of the following: Dr. Nathan R. Wilson, Massachusetts Institute of Technology, 46-6227, 77 Massachusetts Avenue, Cambridge, MA 02139, Email: nathan1{at}mit.edu; or Dr. Guosong Liu, School of Medicine, Tsinghua University, Beijing 100084, China, E-mail: Email: liu.guosong{at}gmail.com
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From the Cover: Asymmetric disassembly and robustness in declining networks
PNAS, October 28, 2008; 105(43): 16466 - 16471.
[Abstract] [Full Text] [PDF]
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