کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2041176 1073150 2015 13 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Disruption of Transient Serotonin Accumulation by Non-Serotonin-Producing Neurons Impairs Cortical Map Development
ترجمه فارسی عنوان
اختلال در تجمع سروتونین گذرا توسط نورونهای تولید کننده غیر ساتونین باعث کاهش رشد نقشه های کرتکت می شود
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم کشاورزی و بیولوژیک (عمومی)
چکیده انگلیسی


• SERT expressed in glutamatergic neuron axons regulates 5-HT in developing CNS
• SERT acts cell autonomously to dictate TCA patterning in sensory cortex
• SERT expressed in TCA shapes spatial organizations of cortical neurons
• Knockout of SERT in TCAs causes excessive 5-HT signals disrupting sensory maps

SummaryPolymorphisms that alter serotonin transporter SERT expression and functionality increase the risks for autism and psychiatric traits. Here, we investigate how SERT controls serotonin signaling in developing CNS in mice. SERT is transiently expressed in specific sets of glutamatergic neurons and uptakes extrasynaptic serotonin during perinatal CNS development. We show that SERT expression in glutamatergic thalamocortical axons (TCAs) dictates sensory map architecture. Knockout of SERT in TCAs causes lasting alterations in TCA patterning, spatial organizations of cortical neurons, and dendritic arborization in sensory cortex. Pharmacological reduction of serotonin synthesis during the first postnatal week rescues sensory maps in SERTGluΔ mice. Furthermore, knockdown of SERT expression in serotonin-producing neurons does not impair barrel maps. We propose that spatiotemporal SERT expression in non-serotonin-producing neurons represents a determinant in early life genetic programming of cortical circuits. Perturbing this SERT function could be involved in the origin of sensory and cognitive deficits associated with neurodevelopmental disorders.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 10, Issue 3, 20 January 2015, Pages 346–358
نویسندگان
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