Research Report Input-rate modulation of gamma oscillations is sensitive to network topology, delays and short-term plasticity Mark D. McDonnell a, , Ashutosh Mohan b , Christian Stricker b , Lawrence M. Ward c a Computational & Theoretical Neuroscience Laboratory, Institute for Telecommunications Research, University of South Australia, Mawson Lakes, SA 5095, Australia b John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia c Department of Psychology and Brain Research Centre, University of British, Columbia, Vancouver, Canada ARTICLE INFO ABSTRACT Article history: Accepted 30 August 2011 Available online 8 September 2011 Simulated networks of excitatory and inhibitory neurons have previously been shown to reproduce critical features of experimental data regarding neural coding in V1, such as a positive relationship between thalamic input spike rate and the power of gamma frequency oscillations. This effect, referred to as modulated gamma power, could represent a neural code in V1 for stimulus characteristics that affect thalamic spike rate such as contrast or intensity. The simulated network's assumptions included homogeneous random connectivity, equal synaptic delays after spike arrival, and constant synaptic efficacies. Plausible alternative assumptions include small world connectivity, a wide distribution of axonal propagation delays, and short term synaptic plasticity, and here we assess the individual impact of each of these on the model's success in reproducing modulated gamma power. First, we developed several alternative algorithms for simulating directed networks with clustered connectivity and balanced excitation and inhibition. We found that modulated gamma power was absent in all small-world networks that had a relatively low abundance of reciprocal connectivity, which suggests that such motifs are present in V1 cortical networks at levels at least equal to those found in random networks. We also found in a different network type that the balance of excitation and inhibition could be destroyed when the network was in the small-world regime. Given all neurons had identical in-degrees, this result suggests that balance relies on motif distributions as well as mean connectivity. Second, altering the distribution of axonal delays had little effect, but increasing the mean delay led to a secondary gamma modulation at harmonics of the main peak, and since this is not observed experimentally, it suggests a mean delay in V1 networks less than 2 ms. Finally, we compared two types of excitatory synap- tic plasticity, and found that modulated beta power emerged in addition to gamma power for one type, in the presence of short term depression in interneurons. This article is part of a Special Issue entitled Neural Coding. © 2011 Elsevier B.V. All rights reserved. Keywords: Directed small world network Cortical connectivity Short term plasticity Axonal delay Local field potential Gamma rhythm BRAIN RESEARCH 1434 (2012) 162 177 Corresponding author. Fax: +61 8 8302 3817. E-mail address: mark.mcdonnell@unisa.edu.au (M.D. McDonnell). 0006-8993/$ see front matter © 2011 Elsevier B.V. All rights reserved. doi:10.1016/j.brainres.2011.08.070 Available online at www.sciencedirect.com www.elsevier.com/locate/brainres