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The Journal of Neuroscience, February 13, 2008, 28(7):1709-1720; doi:10.1523/JNEUROSCI.4263-07.2008

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Neurobiology of Disease
Pathological Effect of Homeostatic Synaptic Scaling on Network Dynamics in Diseases of the Cortex

Flavio Fröhlich,^1,2 Maxim Bazhenov,¹ and Terrence J. Sejnowski^1,2

¹Howard Hughes Medical Institute, The Salk Institute for Biological Studies, Computational Neurobiology Laboratory, La Jolla, California 92037, and ²Division of Biological Sciences, Section of Neurobiology, University of California San Diego, La Jolla, California 92093

Correspondence should be addressed to Dr. Maxim Bazhenov, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037. Email: bazhenov{at}salk.edu

Slow periodic EEG discharges are common in CNS disorders. The pathophysiology of this aberrant rhythmic activity is poorly understood. We used a computational model of a neocortical network with a dynamic homeostatic scaling rule to show that loss of input (partial deafferentation) can trigger network reorganization that results in pathological periodic discharges. The decrease in average firing rate in the network by deafferentation was compensated by homeostatic synaptic scaling of recurrent excitation among pyramidal cells. Synaptic scaling succeeded in recovering the network target firing rate for all degrees of deafferentation (fraction of deafferented cells), but there was a critical degree of deafferentation for pathological network reorganization. For deafferentation degrees below this value, homeostatic upregulation of recurrent excitation had minimal effect on the macroscopic network dynamics. For deafferentation above this threshold, however, a slow periodic oscillation appeared, patterns of activity were less sparse, and bursting occurred in individual neurons. Also, comparison of spike-triggered afferent and recurrent excitatory conductances revealed that information transmission was strongly impaired. These results suggest that homeostatic plasticity can lead to secondary functional impairment in case of cortical disorders associated with cell loss.

Key words: cortex; EEG; encephalopathy; encephalitis; cerebral damage; deafferentation; computational model; homeostatic plasticity; periodic complexes; Alzheimer's disease; Creutzfeldt-Jakob disease

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Received Sept. 17, 2007; revised Nov. 27, 2007; accepted Dec. 17, 2007.

Correspondence should be addressed to Dr. Maxim Bazhenov, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037. Email: bazhenov{at}salk.edu

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