Emergence of synchronicity in a self-organizing spiking neuron network: an approach via genetic algorithms

Soares, Gabriela; Borges, Henrique E.; Gomes, Rogério Martins; Zeferino, Gustavo M.; Braga, Antônio de Pádua

doi:10.1007/s11047-011-9288-3

Cited by 4 publications

(2 citation statements)

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“…We notice that the role of the neuron cooperation is also recognized by Soares et al (2011) who propose the creation of coupled networks to make a significant progress toward the creation of intelligent systems.…”

Section: Discussionsupporting

confidence: 55%

From Self-Organized to Extended Criticality

et al. 2012

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We address the issue of criticality that is attracting the attention of an increasing number of neurophysiologists. Our main purpose is to establish the specific nature of some dynamical processes that although physically different, are usually termed as “critical,” and we focus on those characterized by the cooperative interaction of many units. We notice that the term “criticality” has been adopted to denote both noise-induced phase transitions and Self-Organized Criticality (SOC) with no clear connection with the traditional phase transitions, namely the transformation of a thermodynamic system from one state of matter to another. We notice the recent attractive proposal of extended criticality advocated by Bailly and Longo, which is realized through a wide set of critical points rather than emerging as a singularity from a unique value of the control parameter. We study a set of cooperatively firing neurons and we show that for an extended set of interaction couplings the system exhibits a form of temporal complexity similar to that emerging at criticality from ordinary phase transitions. This extended criticality regime is characterized by three main properties: (i) In the ideal limiting case of infinitely large time period, temporal complexity corresponds to Mittag-Leffler complexity; (ii) For large values of the interaction coupling the periodic nature of the process becomes predominant while maintaining to some extent, in the intermediate time asymptotic region, the signature of complexity; (iii) Focusing our attention on firing neuron avalanches, we find two of the popular SOC properties, namely the power indexes 2 and 1.5 respectively for time length and for the intensity of the avalanches. We derive the main conclusion that SOC emerges from extended criticality, thereby explaining the experimental observation of Plenz and Beggs: avalanches occur in time with surprisingly regularity, in apparent conflict with the temporal complexity of physical critical points.

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Section: Discussionsupporting

confidence: 55%

From Self-Organized to Extended Criticality

et al. 2012

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“…Interestingly, high and low activity states were increased in the presence of Aβ peptide 6 mpi, however, the number of synchronous peaks was robustly decreased. Computational and experimental studies had established that a neuronal group is the most fundamental unit in the cortex and it is not formed by a single neuron, but by a cluster of tightly coupled neural cells, which fire in synchrony [ 53 ]. We have previously shown that nicotinic acetylcholine receptors (nAChRs) are specifically required for synchronized activity patterns in the mouse PFC [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Early and progressive deficit of neuronal activity patterns in a model of local amyloid pathology in mouse prefrontal cortex

Koukouli

Rooy

Maskos

2016

Aging

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Alzheimer's Disease (AD) is the most common form of dementia. The condition predominantly affects the cerebral cortex and hippocampus and is characterized by the spread of amyloid plaques and neurofibrillary tangles (NFTs). But soluble amyloid-β (Aβ) oligomers have also been identified to accumulate in the brains of AD patients and correlate with cognitive dysfunction more than the extent of plaque deposition. Here, we developed an adeno-associated viral vector expressing the human mutated amyloid precursor protein (AAV-hAPP). Intracranial injection of the AAV into the prefrontal cortex (PFC) allowed the induction of AD-like deficits in adult mice, thereby modelling human pathology. AAV-hAPP expression caused accumulation of Aβ oligomers, microglial activation, astrocytosis and the gradual formation of amyloid plaques and NFTs. In vivo two-photon imaging revealed an increase in neuronal activity, a dysfunction characteristic of the pathology, already during the accumulation of soluble oligomers. Importantly, we found that Aβ disrupts the synchronous spontaneous activity of neurons in PFC that, as in humans, is characterized by ultraslow fluctuation patterns. Our work allowed us to track brain activity changes during disease progression and provides new insight into the early deficits of synchronous ongoing brain activity, the “default network”, in the presence of Aβ peptide.

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