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Fig. 1 | BMC Neuroscience

Fig. 1

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

Fig. 1

Hypothetical synaptic variations of 3 monoamines average levels (5-HT, DA, NE) in a lineage of neurons the first generations of which undergo a temporary excess of MAOA (labelled here: MAOA+) during gestation. The impact of two drugs intended for restoring balance of these monoamines is displayed on the right-hand side, including in unaffected neurons (lower curves). Red dots show the monoamine levels outside of their core range (green areas). Red dots with a green outline correspond to out-of-range values which however still respect the coupling of 5-HT and NE monoamines. t1 Beginning of MAOA disruption. t2 Epigenetic regulation of every monoamine. t3 End of the disruptive episode, no later than the end of gestation. t4 Regulation of DA and NE metabolisms by the COMT enzyme as a function of its phenotype (lowest expression with AA, highest with GG). Year 2: The MAOB enzyme is reaching a stage in its rise. Autism symptoms start emerging with a specific pattern of monoamines (indicated by a pink rectangle with an arrow pointing upward to the ASD rise). t5 Decrease of the 5-HT noise by a MOAO inducer which causes some hyperactivity associated with DA and NE deficits. t6 Medication of a low-dose psychostimulant against hyperactivity. The two curves at the bottom show the theoretical effect of the treatment in unaffected neurons, eventually resulting in enhanced metabolism of serotonin

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