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首页> 外文期刊>Journal of communication disorders >A translational approach to vocalization deficits and neural recovery after behavioral treatment in Parkinson disease.
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A translational approach to vocalization deficits and neural recovery after behavioral treatment in Parkinson disease.

机译：帕金森病行为治疗后发声障碍和神经恢复的一种翻译方法。

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Parkinson disease is characterized by a complex neuropathological profile that primarily affects dopaminergic neural pathways in the basal ganglia, including pathways that modulate cranial sensorimotor functions such as swallowing, voice and speech. Prior work from our lab has shown that the rat model of unilateral 6-hydroxydopamine infusion to the medial forebrain bundle that is useful for studying limb sensorimotor deficits also yields vocalization deficits that may be amenable to treatment with intensive exercise. This affords us an opportunity to explore the potential mechanisms underlying behavioral and neural recovery as a result of intervention for cranial sensorimotor deficits associated with Parkinson disease. Our methods include recording and acoustic analysis of male rat ultrasonic vocalizations in a control condition, after neurotoxin infusion (Parkinson disease model), and after targeted vocalization training. We also use well-established behavioral and immunohistochemical methods to assess the level of neurochemical recovery in the striatum of the basal ganglia after our interventions. Our findings, although preliminary, prompt us to look in other brain regions extraneous to the striatum for potential underlying mechanisms of recovery. Thus, our future work will focus on the underlying mechanisms of behavioral recovery in a Parkinson disease model in the hope that this will lead to improved understanding of brain function and improved treatment for voice and swallowing disorders. LEARNING OUTCOMES: Readers will gain an understanding of how a rat model of Parkinson disease is used to study vocalization deficits and interventions.
机译：帕金森氏病的特征是复杂的神经病理学特征，主要影响基底神经节的多巴胺能神经通路，包括调节颅内感觉运动功能（如吞咽，声音和言语）的通路。我们实验室的先前工作表明，将单侧6-羟基多巴胺输注到前脑内侧束的大鼠模型可用于研究肢体感觉运动功能障碍，但也会产生发声障碍，可通过剧烈运动进行治疗。这使我们有机会探索行为和神经恢复的潜在机制，这是干预与帕金森氏病相关的颅感觉运动缺陷的结果。我们的方法包括在控制条件下，在注入神经毒素（帕金森病模型）和有针对性的发声训练后，在控制条件下对雄性大鼠超声发声进行记录和声学分析。我们还使用了完善的行为和免疫组化方法来评估干预后基底神经节纹状体中神经化学恢复的水平。我们的发现尽管是初步的，但仍促使我们在纹状体之外的其他大脑区域中寻找潜在的潜在恢复机制。因此，我们未来的工作将集中在帕金森病模型中行为恢复的潜在机制上，希望这将导致对脑功能的更好理解以及对声音和吞咽障碍的更好治疗。学习成果：读者将了解如何使用帕金森氏病大鼠模型研究发声缺陷和干预措施。

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