沙利度胺诱发自闭症模型大鼠听觉脑干神经元活动的改变

L. E. Tsugiyama, Michiru Ida-Eto, Takeshi Ohkawara, Y. Noro, M. Narita
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引用次数: 6

摘要

自闭症患者的听觉超敏反应在临床上经常被观察到。听觉脑干功能障碍已被怀疑。我们利用产前沙利度胺暴露建立了自闭症模型大鼠。我们研究了自闭症模型大鼠在声音刺激后脑干是否发生异常反应。在妊娠大鼠胚胎第9天和第10天,通过产前暴露沙利度胺制备自闭症模型大鼠。然后,将小鼠置于16 kHz纯音听觉刺激下,并在出生后第49 - 51天进行c - Fos免疫染色检测神经元活动。声音刺激后,自闭症模型大鼠梯形体内侧核的c‐Fos‐阳性神经元数量明显高于对照大鼠。这些结果表明,产前沙利度胺可能导致听觉刺激处理的改变,导致自闭症的听觉超敏特征。
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Altered neuronal activity in the auditory brainstem following sound stimulation in thalidomide‐induced autism model rats
Auditory hypersensitivity in autism is frequently observed in clinics. Dysfunction in the auditory brainstem has been suspected. We have established autism model rats using prenatal thalidomide exposure. Here we investigated whether abnormal response occurs in the brainstem following sound stimulus in autism model rats. Autism model rats were prepared by prenatal exposure to thalidomide on embryonic days 9 and 10 in pregnant rats. Then, the animals were exposed to 16‐kHz pure tone auditory stimulus and c‐Fos immunostaining was performed to examine the neuronal activity on postnatal day 49 to 51. Following sound stimulus, increased number of c‐Fos‐positive neurons was observed in the medial nucleus of the trapezoid body of autism model rats compared with the control rats. These results suggest that prenatal thalidomide might cause altered processing of auditory stimulus, leading to the characteristics of auditory hypersensitivity in autism.
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Obituary for Dr. Robert L. Brent. Altered neuronal activity in the auditory brainstem following sound stimulation in thalidomide‐induced autism model rats A female patient with X‐linked Ohdo syndrome of the Maat‐Kievit‐Brunner phenotype caused by a novel variant of MED12 Low‐prevalence mosaicism of chromosome 18q distal deletion identified by exome‐based copy number profiling in a child with cerebral hypomyelination Tracheal cartilaginous sleeve in patients with Beare‐Stevenson syndrome
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