- AutorIn
- Mareike Fauser
- Francisco Pan-Montojo
- Christian Richter
- Philipp J. Kahle
- Sigrid C. Schwarz
- Johannes Schwarz
- Alexander Storch
- Andreas Hermann
- Titel
- Chronic–Progressive Dopaminergic Deficiency Does Not Induce Midbrain Neurogenesis
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:15-qucosa2-851196
- Quellenangabe
- Cells : open access journal
Erscheinungsjahr: 2021
Jahrgang: 10
Heft: 4
E-ISSN: 2073-4409
Artikelnummer: 775 - Erstveröffentlichung
- 2021
- Abstract (EN)
- 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.
- Andere Ausgabe
- Link zur Erstveröffentlichung
Link: https://doi.org/10.3390/cells10040775 - Freie Schlagwörter (EN)
- adult neurogenesis; periventricular regions; non-neurogenic regions; Parkinson´s disease; dopaminergic neurodegeneration; transgenic animal model
- Klassifikation (DDC)
- 570
- Verlag
- MDPI, Basel
- Version / Begutachtungsstatus
- publizierte Version / Verlagsversion
- URN Qucosa
- urn:nbn:de:bsz:15-qucosa2-851196
- Veröffentlichungsdatum Qucosa
- 03.05.2023
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
- CC BY 4.0