2010
DOI: 10.1007/s10827-010-0256-1
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Can homeostatic plasticity in deafferented primary auditory cortex lead to travelling waves of excitation?

Abstract: Travelling waves of activity in neural circuits have been proposed as a mechanism underlying a variety of neurological disorders, including epileptic seizures, migraine auras and brain injury. The highly influential Wilson-Cowan cortical model describes the dynamics of a network of excitatory and inhibitory neurons. The Wilson-Cowan equations predict travelling waves of activity in rate-based models that have sufficiently reduced levels of lateral inhibition. Travelling waves of excitation may play a role in f… Show more

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Cited by 40 publications
(40 citation statements)
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“…Schaette and Kempter (2006) and more recently Noreña (2011) advanced this concept by suggesting that a “homeostatic plasticity mechanism” stabilizes the mean firing rates of CAS neurons around a set point value. Computational studies by Schaette and Kempter (2006), Chrostowski et al (2011), and Noreña (2011) confirm that such a mechanism could explain the increased spontaneous activity that occurs (e.g., in the DCN) in response to sensory deprivation. With this neural homeostasis model, a damaged cochlea would result in reduced output from the auditory nerve, which would, in turn, trigger the amplification of “neural noise,” which would be perceived as tinnitus.…”
Section: Neural Models Of Tinnitusmentioning
confidence: 81%
“…Schaette and Kempter (2006) and more recently Noreña (2011) advanced this concept by suggesting that a “homeostatic plasticity mechanism” stabilizes the mean firing rates of CAS neurons around a set point value. Computational studies by Schaette and Kempter (2006), Chrostowski et al (2011), and Noreña (2011) confirm that such a mechanism could explain the increased spontaneous activity that occurs (e.g., in the DCN) in response to sensory deprivation. With this neural homeostasis model, a damaged cochlea would result in reduced output from the auditory nerve, which would, in turn, trigger the amplification of “neural noise,” which would be perceived as tinnitus.…”
Section: Neural Models Of Tinnitusmentioning
confidence: 81%
“…On the other hand it is possible that psychological stress, current or previous psychiatric disorders, and personality traits associated with a genetically or epigenetically determined vulnerability may represent a vulnerability factor giving rise to maladaptive tinnitus-related neuroplastic rearrangements [135] leading to tinnitus symptomatology. Given the above, our hypothesis is that patients' symptomatology may be considered the peculiar expression of an alteration of global brain hodological equilibrium.…”
Section: Discussionmentioning
confidence: 99%
“…These changes can be classed as dynamic modulations of spontaneous and driven neural activity, the underpinnings of which appear to rely upon putatively homeostatic gain-modulation mechanisms that affect the extent of neural excitability, and selectively modulate the balance of excitation and inhibition. Changes at the single neuron and network processing levels can be demonstrated in vivo (e.g., Noreña, 2011; Yang et al, 2011, 2012) and by in silico modeling (Dominguez et al, 2006; Schaette and Kempter, 2006, 2008, 2012; Chrostowski et al, 2011; Tass and Popovych, 2012; Schaette, 2013). Although these neurophysiological sequelae are becoming better understood, it remains an ongoing problem as to whether the various components of central modulation, at different levels of the auditory pathway, might translate into perceptual abnormalities, like tinnitus, that could interrogated by behavioral testing.…”
Section: The Functional and Behavioral Implications Of Trauma-driven mentioning
confidence: 99%