Graduate Neuroscience Program, University of California, Riverside, USA.
Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, USA.
J Neurodev Disord. 2023 Jul 29;15(1):23. doi: 10.1186/s11689-023-09496-8.
Autism spectrum disorders (ASD) encompass a wide array of debilitating symptoms, including sensory dysfunction and delayed language development. Auditory temporal processing is crucial for speech perception and language development. Abnormal development of temporal processing may account for the language impairments associated with ASD. Very little is known about the development of temporal processing in any animal model of ASD.
In the current study, we quantify auditory temporal processing throughout development in the Fmr1 knock-out (KO) mouse model of Fragile X Syndrome (FXS), a leading genetic cause of intellectual disability and ASD-associated behaviors. Using epidural electrodes in awake and freely moving wildtype (WT) and KO mice, we recorded auditory event related potentials (ERP) and auditory temporal processing with a gap-in-noise auditory steady state response (gap-ASSR) paradigm. Mice were recorded at three different ages in a cross sectional design: postnatal (p)21, p30 and p60. Recordings were obtained from both auditory and frontal cortices. The gap-ASSR requires underlying neural generators to synchronize responses to gaps of different widths embedded in noise, providing an objective measure of temporal processing across genotypes and age groups.
We present evidence that the frontal, but not auditory, cortex shows significant temporal processing deficits at p21 and p30, with poor ability to phase lock to rapid gaps in noise. Temporal processing was similar in both genotypes in adult mice. ERP amplitudes were larger in Fmr1 KO mice in both auditory and frontal cortex, consistent with ERP data in humans with FXS.
These data indicate cortical region-specific delays in temporal processing development in Fmr1 KO mice. Developmental delays in the ability of frontal cortex to follow rapid changes in sounds may shape language delays in FXS, and more broadly in ASD.
自闭症谱系障碍(ASD)包括广泛的致残症状,包括感觉功能障碍和语言发育迟缓。听觉时间处理对于言语感知和语言发展至关重要。时间处理的异常发育可能解释了与 ASD 相关的语言障碍。在任何 ASD 的动物模型中,关于时间处理的发展,人们知之甚少。
在目前的研究中,我们在脆性 X 综合征(FXS)的 Fmr1 敲除(KO)小鼠模型中,定量了听觉时间处理在整个发育过程中的发展,FXS 是智力障碍和 ASD 相关行为的主要遗传原因。我们在清醒和自由移动的野生型(WT)和 KO 小鼠中使用硬膜外电极,使用噪声中的间隙听觉稳态反应(gap-ASSR)范式记录听觉事件相关电位(ERP)和听觉时间处理。我们以横向设计在三个不同的年龄记录小鼠:出生后(p)21、p30 和 p60。从听觉和额叶皮层获得记录。gap-ASSR 需要潜在的神经发生器对嵌入噪声中的不同宽度的间隙响应进行同步,为跨基因型和年龄组的时间处理提供客观的衡量标准。
我们提供的证据表明,额叶而不是听觉皮层在 p21 和 p30 时显示出明显的时间处理缺陷,对噪声中快速间隙的相位锁定能力差。在成年小鼠中,两种基因型的时间处理都相似。在听觉和额叶皮层中,Fmr1 KO 小鼠的 ERP 振幅均较大,与 FXS 患者的 ERP 数据一致。
这些数据表明,Fmr1 KO 小鼠的额叶皮质时间处理发育存在区域特异性延迟。额叶皮层跟随声音快速变化的能力延迟可能会导致 FXS 中的语言延迟,更广泛地说,在 ASD 中也是如此。