From Forced to Natural Competition in a Biologically Plausible Neural Network

Peláez, Francisco Javier Ropero; Godoi, Antonio Carlos

doi:10.1007/978-3-642-35230-0_10

Cited by 2 publications

(3 citation statements)

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“…As mentioned in Introduction, this research study is based on a computational model of the cerebral koniocortex that we developed in previous work [ 23 , 26 ].…”

Section: Methodsmentioning

confidence: 99%

“…Initially, instead of simulating brain impairment, our priority was to develop operational models of brain structures like the thalamus [ 19 , 20 ], the amygdala [ 21 ], and the koniocortex [ 22 , 23 ]. When their initial operation was satisfactory, the way of further evaluating them was by modeling brain disorders.…”

Section: Introductionmentioning

confidence: 99%

“…A similar strategy allowed the assessment of the circuit linking the thalamus and the amygdala, which led to an effective therapy for treating specific phobias [ 21 ]. We also modeled the koniocortex, the first cortical layer receiving inputs from the sensory thalamus [ 23 , 26 ]. Once modeled, learning emerges competitively with spiny stellate (SS) neurons behaving in a “winner-take-all” (WTA) manner (In a pool of neurons, “winner-take-all” means that the most activated neuron starts firing while the others keep silent.).…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model

Aguiar-Furucho

Peláez

2020

Neural Plasticity

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Several research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer’s disease. To simulate Alzheimer’s disease earlier stages, which manifest in sensory cortices, we used a computational model of the koniocortex that is the first cortical stage processing sensory information. The architecture and physiology of the modeled koniocortex resemble those of its cerebral counterpart being capable of continuous learning. This model allows one to analyze the initial phases of Alzheimer’s disease by “aging” the artificial koniocortex through synaptic pruning, by the modification of acetylcholine and GABA-A signaling, and by reducing sensory stimuli, among other processes. The computational model shows that during aging, a GABA-A deficit followed by a reduction in sensory stimuli leads to a dysregulation of neural excitability, which in the biological brain is associated with hypermetabolism, one of the earliest symptoms of Alzheimer’s disease.

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“…As mentioned in Introduction, this research study is based on a computational model of the cerebral koniocortex that we developed in previous work [ 23 , 26 ].…”

Section: Methodsmentioning

confidence: 99%