کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6273945 1614809 2014 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
ReviewThe developmental disruptions of serotonin signaling may involved in autism during early brain development
ترجمه فارسی عنوان
اختلالات رشدی سیگنالینگ سروتونین ممکن است در طی اوتیسم مغزی درگیر در اوتیسم باشد
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


- Developmental disruptions of serotonin signaling involved in autism.
- Hyperserotonemia provokes a loss of serotonin terminals.
- Deficiency of the serotonergic system induces mis-wiring of neural network.

Autism is a developmental disorder defined by the presence of a triad of communication, social and stereo typical behavioral characteristics with onset before 3 years of age. In spite of the fact that there are potential environmental factors for autistic behavior, the dysfunction of serotonin during early development of the brain could be playing a role in this prevalence rise. Serotonin can modulate a number of developmental events, including cell division, neuronal migration, cell differentiation and synaptogenesis. Hyperserotonemia during fetal development results in the loss of serotonin terminals through negative feedback. The increased serotonin causes a decrease of oxytocin in the paraventricular nucleus of the hypothalamus and an increase in calcitonin gene-related peptide (CGRP) in the central nucleus of the amygdale, which are associated with social interactions and vital in autism. However, hyposerotonemia may be also relevant to the development of sensory as well as motor and cognitive faculties. And the paucity of placenta-derived serotonin should have potential importance when the pathogenesis of autism is considered. This review briefly summarized the developmental disruptions of serotonin signaling involved in the pathogenesis of autism during early development of the brain.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 267, 16 May 2014, Pages 1-10
نویسندگان
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