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肌张力障碍大鼠的发声发育

Vocal development in dystonic rats.

作者信息

Riede Tobias, Zhao Yu, LeDoux Mark S

机构信息

Department of Physiology, Midwestern University, Glendale, Arizona

Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee.

出版信息

Physiol Rep. 2015 Apr;3(4). doi: 10.14814/phy2.12350.

Abstract

Vocal production, which requires the generation and integration of laryngeal and respiratory motor patterns, can be impaired in dystonia, a disorder believed due to dysfunction of sensorimotor pathways in the central nervous system. Herein, we analyze vocal and respiratory abnormalities in the dystonic (dt) rat, a well-characterized model of generalized dystonia. The dt rat is a recessive mutant with haploinsufficiency of Atcay which encodes the neuronally restricted protein caytaxin. Olivocerebellar functional abnormalities are central to the dt rat's truncal and appendicular dystonia and could also contribute to vocal and respiratory abnormalities in this model system. Differences in vocal repertoire composition were found between homozygote and wild-type dt rat pups developing after 3 weeks of life. Those spectro-temporal differences were not paralleled by differences in vocal activity or maximum lung pressures during quiet breathing and vocalization. However, breathing rhythm was slower in homozygote pups. This slower breathing rhythm persisted into adulthood. Given that cerebellectomy eliminates truncal and appendicular dystonia in the dt rat, we hypothesize that the altered breathing patterns stem either from a disturbance in the maturation of respiratory pattern generators or from deficient extracerebellar caytaxin expression affecting normal respiratory pattern generation. The altered breathing rhythm associated with vocal changes in the murine model resembles aspects of vocal dysfunction that are seen in humans with sporadic dystonia.

摘要

发声需要产生并整合喉部和呼吸运动模式,而在肌张力障碍中可能会受损,肌张力障碍是一种被认为由中枢神经系统感觉运动通路功能障碍引起的疾病。在此,我们分析了肌张力障碍(dt)大鼠的发声和呼吸异常,dt大鼠是一种特征明确的全身性肌张力障碍模型。dt大鼠是一种隐性突变体,Atcay基因单倍剂量不足,Atcay基因编码神经元限制性蛋白caytaxin。橄榄小脑功能异常是dt大鼠躯干和肢体肌张力障碍的核心,也可能导致该模型系统中的发声和呼吸异常。在出生3周后发育的纯合子和野生型dt大鼠幼崽之间,发现了发声 repertoire 组成的差异。这些频谱-时间差异与安静呼吸和发声时的发声活动或最大肺压差异并不平行。然而,纯合子幼崽的呼吸节律较慢。这种较慢的呼吸节律持续到成年。鉴于小脑切除可消除dt大鼠的躯干和肢体肌张力障碍,我们推测呼吸模式的改变要么源于呼吸模式发生器成熟过程中的紊乱,要么源于影响正常呼吸模式生成的小脑外caytaxin表达不足。小鼠模型中与发声变化相关的呼吸节律改变类似于散发性肌张力障碍患者中所见的发声功能障碍的某些方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fb0/4425958/bd696045c34a/phy20003-e12350-f1.jpg

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