Human fetal dopamine neurons grafted in a rat model of Parkinson's disease: ultrastructural evidence for synapse formation using tyrosine hydroxylase immunocytochemistry

1988 ◽  
Vol 73 (1) ◽  
pp. 115-126 ◽  
Author(s):  
D. J. Clarke ◽  
P. Brundin ◽  
R. E. Strecker ◽  
O. G. Nilsson ◽  
A. Bj�rklund ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Tyrosine Hydroxylase ◽  
Rat Model ◽  
Synapse Formation ◽  
Dopamine Neurons ◽  
Ultrastructural Evidence ◽  
Tyrosine Hydroxylase Immunocytochemistry

scholarly journals Human ESC-Derived Dopamine Neurons Show Similar Preclinical Efficacy and Potency to Fetal Neurons when Grafted in a Rat Model of Parkinson’s Disease

2014 ◽  
Vol 15 (5) ◽  
pp. 653-665 ◽  
Author(s):  
Shane Grealish ◽  
Elsa Diguet ◽  
Agnete Kirkeby ◽  
Bengt Mattsson ◽  
Andreas Heuer ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Dopamine Neurons ◽  
Preclinical Efficacy

Behavioural effects of human fetal dopamine neurons grafted in a rat model of Parkinson's disease

1986 ◽  
Vol 65 (1) ◽  
Author(s):  
P. Brundin ◽  
O.G. Nilsson ◽  
R.E. Strecker ◽  
O. Lindvall ◽  
B. �stedt ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Dopamine Neurons ◽  
Behavioural Effects

Interference with anoikis-induced cell death of dopamine neurons: Implications for augmenting embryonic graft survival in a rat model of Parkinson's disease

2003 ◽  
Vol 464 (2) ◽  
pp. 172-179 ◽  
Author(s):  
Deanna M. Marchionini ◽  
Timothy J. Collier ◽  
Maria Camargo ◽  
Susan McGuire ◽  
Mark Pitzer ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Graft Survival ◽  
Rat Model ◽  
Dopamine Neurons

scholarly journals Functional and behavioral consequences of Parkinson's disease-associated LRRK2-G2019S mutation

2018 ◽  
Vol 46 (6) ◽  
pp. 1697-1705 ◽  
Author(s):  
Deanna L. Benson ◽  
Bridget A. Matikainen-Ankney ◽  
Ayan Hussein ◽  
George W. Huntley
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Social Stress ◽  
Synapse Formation ◽  
Neural Circuits ◽  
Brain Regions ◽  
Synaptic Activity ◽  
Dopamine Neurons ◽  
Lrrk2 Mutation ◽  
Lrrk2 G2019s

LRRK2 mutation is the most common inherited, autosomal dominant cause of Parkinson's disease (PD) and has also been observed in sporadic cases. Most mutations result in increased LRRK2 kinase activity. LRRK2 is highly expressed in brain regions that receive dense, convergent innervation by dopaminergic and glutamatergic axons, and its levels rise developmentally coincident with glutamatergic synapse formation. The onset and timing of expression suggests strongly that LRRK2 regulates the development, maturation and function of synapses. Several lines of data in mice show that LRRK2-G2019S, the most common LRRK2 mutation, produces an abnormal gain of pathological function that affects synaptic activity, spine morphology, persistent forms of synapse plasticity and behavioral responses to social stress. Effects of the mutation can be detected as early as the second week of postnatal development and can last or have consequences that extend into adulthood and occur in the absence of dopamine loss. These data suggest that the generation of neural circuits that support complex behaviors is modified by LRRK2-G2019S. Whether such alterations impart vulnerability to neurons directly or indirectly, they bring to the forefront the idea that neural circuits within which dopamine neurons eventually degenerate are assembled and utilized in ways that are distinct from circuits that lack this mutation and may contribute to non-motor symptoms observed in humans with PD.

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