Abstract
Even without external random input, cortical networks in vivo sustain asynchronous irregular firing with low firing rate. In addition to detailed balance between excitatory and inhibitory activities, recent theoretical studies have revealed that another feature commonly observed in cortical networks, i.e., long-tailed distribution of excitatory synapses implying coexistence of many weak and a few extremely strong excitatory synapses, plays an essential role in realizing the self-sustained activity in recurrent networks of biologically plausible spiking neurons. The previous studies, however, have not considered highly non-random features of the synaptic connectivity, namely, bidirectional connections between cortical neurons are more common than expected by chance and strengths of synapses are positively correlated between pre- and postsynaptic neurons. The positive correlation of synaptic connections may destabilize asynchronous activity of networks with the long-tailed synaptic distribution and induce pathological synchronized firing among neurons. It remains unclear how the cortical network avoids such pathological synchronization. Here, we demonstrate that introduction of the correlated connections indeed gives rise to synchronized firings in a cortical network model with the long-tailed distribution. By using a simplified feed-forward network model of spiking neurons, we clarify the underlying mechanism of the synchronization. We then show that the synchronization can be efficiently suppressed by highly heterogeneous distribution, typically a lognormal distribution, of inhibitory-to-excitatory connection strengths in a recurrent network model of cortical neurons.
Highlights
Sustained asynchronous irregular activity of cortical neurons is commonly observed in cell cultures (Gross et al, 1982; Plenz and Aertsen, 1996; Marom and Shahaf, 2002), in vitro (Mao et al, 2001; Shu et al, 2003b), and in vivo (Timofeev et al, 2000) even in the absence of external stimuli
The spike timings are highly correlated among neurons in the network with R = 0.35, whereas uncorrelated neural firings are observed with R = 0.0. This implies that normal firing state of the cortex is replaced by pathological synchronization among neurons as bidirectional correlation is introduced to the model networks, even though the bidirectional connections are considered biologically plausible
Pathological synchronization of spontaneous firings and a possible mechanism to suppress them in a cortical network model with biologically plausible nonrandom features of connectivity has been investigated
Summary
Sustained asynchronous irregular activity of cortical neurons is commonly observed in cell cultures (Gross et al, 1982; Plenz and Aertsen, 1996; Marom and Shahaf, 2002), in vitro (Mao et al, 2001; Shu et al, 2003b), and in vivo (Timofeev et al, 2000) even in the absence of external stimuli. Asynchronous activities of neurons realized in these studies faithfully share various properties with the sustained activity observed in vivo, such as high-irregularity (Softky and Koch, 1993; Stiefel et al, 2013), extremely low firing rate (Hromádka et al, 2008; Mizuseki and Buzsáki, 2013), highconductance membrane potential with large fluctuation (Wilson and Kawaguchi, 1996; Destexhe et al, 2001), and persistent UP state of membrane potential (Steriade et al, 2001; Destexhe et al, 2003; Shu et al, 2003a) In these models, amplitudes of excitatory postsynaptic potentials (EPSP) for excitatory-toexcitatory connections follow a long-tailed distribution, such as the lognormal distribution, with many weak and a few extremely strong synapses, which allows networks to generate and stably maintain the asynchronous irregular activity (Teramae et al, 2012)
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