Dysfunctional striatal dopamine signaling in Huntington's disease
Autor: | Lynn A. Raymond, Ellen T. Koch |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Dopamine Glutamic Acid Substantia nigra Striatum Biology Receptors Dopamine 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Huntington's disease medicine Animals Humans Cerebral Cortex Neurons Huntingtin Protein Dopaminergic Glutamate receptor medicine.disease Corpus Striatum Substantia Nigra Disease Models Animal 030104 developmental biology Huntington Disease Dopamine receptor Signal transduction Neuroscience 030217 neurology & neurosurgery medicine.drug Signal Transduction |
Zdroj: | Journal of neuroscience researchREFERENCES. 97(12) |
ISSN: | 1097-4547 |
Popis: | Dopamine signaling in the striatum is critical for a variety of behaviors including movement, behavioral flexibility, response to reward and many forms of learning. Alterations to dopamine transmission contribute to pathological features of many neurological diseases, including Huntington's disease (HD). HD is an autosomal dominant genetic disorder caused by a CAG repeat expansion in the Huntingtin gene. The striatum is preferentially degenerated in HD, and this region receives dopaminergic input from the substantia nigra. Studies of HD patients and genetic rodent models have shown changes to levels of dopamine and its receptors in the striatum, and alterations in dopamine receptor signaling and modulation of other neurotransmitters, notably glutamate. Throughout his career, Dr. Michael Levine's research has furthered our understanding of dopamine signaling in the striatum of healthy rodents and HD mouse models. This review will focus on the work of his group and others in elucidating alterations to striatal dopamine signaling that contribute to pathophysiology in HD mouse models, and how these findings relate to human HD studies. We will also discuss current and potential therapeutic interventions for HD that target the dopamine system, and future research directions for this field. |
Databáze: | OpenAIRE |
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