A mouse model for tracking nigrostriatal dopamine neuron axon growth

genesis ◽  
2008 ◽  
Vol 46 (3) ◽  
pp. 125-131 ◽  
Author(s):  
Joaquim Vives ◽  
Piriya Sasajala ◽  
Kuo Hsuan Chang ◽  
Suling Zhao ◽  
Meng Li
Keyword(s):  
Mouse Model ◽  
Axon Growth ◽  
Dopamine Neuron ◽  
Nigrostriatal Dopamine

scholarly journals Control of the Nigrostriatal Dopamine Neuron Activity and Motor Function by the Tail of the Ventral Tegmental Area

2014 ◽  
Vol 39 (12) ◽  
pp. 2788-2798 ◽  
Author(s):  
Romain Bourdy ◽  
María-José Sánchez-Catalán ◽  
Jennifer Kaufling ◽  
Judith J Balcita-Pedicino ◽  
Marie-José Freund-Mercier ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Motor Function ◽  
Dopamine Neuron ◽  
Neuron Activity ◽  
Nigrostriatal Dopamine ◽  
Ventral Tegmental

Prevention and restoration of lactacystin‐induced nigrostriatal dopamine neuron degeneration by novel brain‐permeable iron chelators

2007 ◽  
Vol 21 (14) ◽  
pp. 3835-3844 ◽  
Author(s):  
Wen Zhu ◽  
Wenjie Xie ◽  
Tianhong Pan ◽  
Pingyi Xu ◽  
Mati Fridkin ◽  
...  
Keyword(s):  
Dopamine Neuron ◽  
Iron Chelators ◽  
Neuron Degeneration ◽  
Nigrostriatal Dopamine ◽  
Permeable Iron

scholarly journals Neurodevelopmental wiring deficits in the Ts65Dn mouse model of Down syndrome

2019 ◽  
Author(s):  
Shruti Jain ◽  
Christina A. Watts ◽  
Wilson C.J. Chung ◽  
Kristy Welshhans
Keyword(s):  
Down Syndrome ◽  
Corpus Callosum ◽  
Mouse Model ◽  
Hippocampal Neurons ◽  
Anterior Commissure ◽  
Axon Growth ◽  
Chromosome 21 ◽  
Ts65dn Mouse ◽  
Hippocampal Commissure ◽  
Interhemispheric Connectivity

AbstractDown syndrome is the most common genetic cause of intellectual disability and occurs due to the trisomy of human chromosome 21. Adolescent and adult brains from humans with Down syndrome exhibit various neurological phenotypes including a reduction in the size of the corpus callosum, hippocampal commissure and anterior commissure. However, it is unclear when and how these interhemispheric connectivity defects arise. Using the Ts65Dn mouse model of Down syndrome, we examined interhemispheric connectivity in postnatal day 0 (P0) Ts65Dn mouse brains. We find that there is no change in the volume of the corpus callosum or anterior commissure in P0 Ts65Dn mice. However, the volume of the hippocampal commissure is significantly reduced in P0 Ts65Dn mice, and this may contribute to the impaired learning and memory phenotype of this disorder. Interhemispheric connectivity defects that arise during development may be due to disrupted axon growth. In line with this, we find that developing hippocampal neurons display reduced axon length in vitro, as compared to neurons from their euploid littermates. This study is the first to report the presence of defective interhemispheric connectivity at the time of birth in Ts65Dn mice, providing evidence that early therapeutic intervention may be an effective time window for the treatment of Down syndrome.

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