Chronic–Progressive Dopaminergic Deficiency Does Not Induce Midbrain Neurogenesis
Autor: | Sigrid C. Schwarz, Mareike Fauser, Johannes Schwarz, Francisco Pan-Montojo, Andreas Hermann, Philipp J. Kahle, Christian Richter, Alexander Storch |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Dopamine Neurogenesis adult neurogenesis periventricular regions non-neurogenic regions Parkinson´s disease dopaminergic neurodegeneration transgenic animal model Hindbrain Biology Receptors Nicotinic physiology [Mesencephalon] Article Midbrain 03 medical and health sciences Lateral ventricles deficiency [Dopamine] 0302 clinical medicine Mesencephalon Dopaminergic Cell Lateral Ventricles ddc:570 medicine Animals Humans metabolism [alpha-Synuclein] lcsh:QH301-705.5 Cell Proliferation physiology [Lateral Ventricles] Dopaminergic Neurodegeneration General Medicine medicine.disease Neural stem cell Rhombencephalon Mice Inbred C57BL 030104 developmental biology nervous system lcsh:Biology (General) metabolism [Receptors Nicotinic] physiology [Rhombencephalon] alpha-Synuclein Neuroscience 030217 neurology & neurosurgery |
Zdroj: | Cells, Vol 10, Iss 775, p 775 (2021) Cells 10(4), 775-(2021). doi:10.3390/cells10040775 Cells Volume 10 Issue 4 |
ISSN: | 2073-4409 |
DOI: | 10.3390/cells10040775 |
Popis: | Background: Consecutive adult neurogenesis is a well-known phenomenon in the ventricular–subventricular zone of the lateral wall of the lateral ventricles (V–SVZ) and has been controversially discussed in so-called “non-neurogenic” brain areas such as the periventricular regions (PVRs) of the aqueduct and the fourth ventricle. Dopamine is a known modulator of adult neural stem cell (aNSC) proliferation and dopaminergic neurogenesis in the olfactory bulb, though a possible interplay between local dopaminergic neurodegeneration and induction of aNSC proliferation in mid/hindbrain PVRs is currently enigmatic. Objective/Hypothesis: To analyze the influence of chronic–progressive dopaminergic neurodegeneration on both consecutive adult neurogenesis in the PVRs of the V–SVZ and mid/hindbrain aNSCs in two mechanistically different transgenic animal models of Parkinson´s disease (PD). Methods: We used Thy1-m[A30P]h α synuclein mice and Leu9′Ser hypersensitive α4* nAChR mice to assess the influence of midbrain dopaminergic neuronal loss on neurogenic activity in the PVRs of the V–SVZ, the aqueduct and the fourth ventricle. Results: In both animal models, overall proliferative activity in the V–SVZ was not altered, though the proportion of B2/activated B1 cells on all proliferating cells was reduced in the V–SVZ in Leu9′Ser hypersensitive α4* nAChR mice. Putative aNSCs in the mid/hindbrain PVRs are known to be quiescent in vivo in healthy controls, and dopaminergic deficiency did not induce proliferative activity in these regions in both disease models. Conclusions: Our data do not support an activation of endogenous aNSCs in mid/hindbrain PVRs after local dopaminergic neurodegeneration. Spontaneous endogenous regeneration of dopaminergic cell loss through resident aNSCs is therefore unlikely. |
Databáze: | OpenAIRE |
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