期刊
NEUROCHEMICAL RESEARCH
卷 47, 期 9, 页码 2558-2567出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-020-03226-5
关键词
Dugesia japonica; Dopaminergic neuron; Regeneration; Mitogen-activated protein kinase; Neoblast
资金
- Smoking Research Foundation
- JSPS KAKENHI, MEXT, Japan [16H07341, 18K06904, 18K15034, 20K16138]
The study revealed the involvement of the MEK/ERK pathway in the regeneration of dopaminergic neurons in planarians, with MEK inhibitors affecting head region morphogenesis and reducing the number of dopaminergic neurons.
Planarian Dugesia japonica is a flatworm that can autonomously regenerate its own body after an artificial amputation. A recent report showed the role of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway in the head morphogenesis during the planarian regeneration process after amputation; however, neuron-specific regeneration mechanisms have not yet been reported. Here, whether MEK/ERK pathway was involved in the dopaminergic neuronal regeneration in planarians was investigated. Planarians regenerated their body within 14 days after amputation; however, the head region morphogenesis was inhibited by MEK inhibitor U0126 (3 or 10 mu M). Furthermore, the number of planarian tyrosine hydroxylase (DjTH)-positive dopaminergic neurons in the regenerated head region was also decreased by U0126. The 6-hydroxydopamine (6-OHDA), a dopaminergic neurotoxin, can decrease the number of dopaminergic neurons; however, planarians can regenerate dopaminergic neurons after injecting 6-OHDA into the intestinal tract. MEK inhibitor PD98059 (30 mu M) or U0126 (10 mu M) significantly decreased dopaminergic neurons 5 days after the 6-OHDA injection. During the regeneration process of dopaminergic neurons, phosphorylated histone H3 (H3P)-positive stem cells known as neoblasts were increased in the head region; however, MEK inhibitors significantly decreased the number of H3P-positive neoblasts. These results suggested that dopaminergic neuronal regeneration in planarian was regulated by the MEK/ERK pathway.
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