http://www.sciencedirect.com/science/article/pii/S2212877816300783
- Under a Creative Commons license
Highlights
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- Acute amylin affected genes involved in pathways and processes that drive neurogenesis.
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- Chronic amylin increased the number of newly proliferating cells in the AP of adult rats.
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- Chronic amylin determined neuronal fate over astrocytes in the AP of adult rats.
Abstract
Objective
Adult
neurogenesis in the subgranular zone and subventricular zone is
generally accepted, but its existence in other brain areas is still
controversial. Circumventricular organs, such as the area postrema
(AP) have recently been described as potential neurogenic niches in the
adult brain. The AP is the major site of action of the satiating
hormone amylin. Amylin has been recently shown to promote the formation
of neuronal projections originating from the AP in neonatal rodents but
the role of amylin in adult neurogenesis remains unknown.
Methods
To
test this, we first performed an RNA-sequencing of the AP of adult rats
acutely injected with either amylin (20 μg/kg), amylin plus the amylin
receptor antagonist AC187 (500 μg/kg) or vehicle. Second, animals were
subcutaneously equipped with minipumps releasing either amylin
(50 μg/kg/day) or vehicle for 3 weeks to assess cell proliferation and
differentiation with the 5′-bromo-2-deoxyuridine (BrdU) technique.
Results
Acute
amylin injections affected genes involved in pathways and processes
that control adult neurogenesis. Amylin consistently upregulated NeuroD1
transcript and protein in the adult AP, and this effect was blocked by
the co-administration of AC187. Further, chronic amylin treatment
increased the number of newly proliferated AP-cells and significantly
promoted their differentiation into neurons rather than astrocytes.
Conclusion
Our findings revealed a novel role of the satiating hormone amylin in promoting neurogenesis in the AP of adult rats.
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