A Functional Model of Fast Action Selection Guided by Emotional Stimuli

Béroule, Dominique; Verrier, Pascale Gisquet

doi:10.4172/2090-4908.1000132

Cited by 1 publication

(3 citation statements)

References 39 publications

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“…6). Furthermore, although aberrant internal representations are not erased, their online access can be repressed through counterconditioning [66]. However, new branches can still sprout from existing over-generalized paths, unless events occur in a context different from all those previously experienced with a w 5ht noise.…”

Section: Resultsmentioning

confidence: 99%

“…The software implemented in this study is derived from the GP model of emotional decision-making [66]. Similarly, the input patterns of activity represent behaviors, while the software output consists of several types of information delivered over a computer session: labels of memory paths whenever they are created, amount of cells and links within/between modules, and activity histograms of selected memory paths.…”

Section: Methodsmentioning

confidence: 99%

“…Based on the same simplified representation of neuromodulation, a computer implementation of decision-making has more recently been designed, in line with the ascending spiral neurobiological model [64]. For this purpose, parallel GP-channels can be connected through cross-circuits aimed at propagating modulating signals from “emotional” to “conditioner” and eventually “sensorimotor” channels where decisions are thus quickly facilitated/repressed [65, 66]. But this anticipation skill brought an inescapable constraint of the original learning algorithm to the surface.…”

Section: Introductionmentioning

confidence: 99%

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Offline encoding impaired by epigenetic regulations of monoamines in the guided propagation model of autism

Béroule

2018

BMC Neurosci

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Background Environmental factors can modify the expression of genes, including those involved in the metabolism of neurotransmitters. Accounting for a control role of monoamine neurotransmitters, the guided propagation (GP) memory model may contribute to investigate the consequences of neuromodulation impairments on development disorders such as autism. A prenatal transient excess of ‘monoamine oxidase A’ enzyme is assumed here to trigger persistent epigenetic regulations that would induce imbalanced metabolisms of synaptic monoamines. When imported into the ‘offline’ encoding cycles of a GP model, the consequent ‘serotoninergic noise’ leads to aberrant memory structures that can be linked with autism symptoms.ResultsIn computer experiments, different levels of uncoupling between representations of monoamines correlate with the amount of impaired GP modules, the severity of irrelevant connections, as well as network overgrowth. Two types of faulty connections are respectively assumed to underlie autism traits, namely repetitive behavior and perceptual oversensitivity. Besides computational modelling, a genetic family-tree shows how the autism sex-ratio can result from combinations of pharmacological and epigenetic features.ConclusionsThese results suggest that the current rise of autism is favored by three possible sources of biological masking: (1) during sleep, when cyclic variations of monoamines may undergo disrupted enzymatic activities; (2) across generations of ‘healthy carriers’ protected by the X-chromosome silencing and a specific genetic variant; (3) early in life, as long as the brain development draws on pools of neurons born when the transient enzymatic excess and its persistent epigenetic regulation overlapped, and as long as the B type of monoamine oxidase does not significantly impact dopamine. A disease-modifying therapy can be derived from this study, which involves relevant biomarkers to be first monitored over several months of clinical trial.Electronic supplementary materialThe online version of this article (10.1186/s12868-018-0477-1) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%