Fauser, Mareike
[Author];
Pan-Montojo, Francisco
[Author];
Richter, Christian
[Author];
Kahle, Philipp J.
[Author];
Schwarz, Sigrid C.
[Author];
Schwarz, Johannes
[Author];
Storch, Alexander
[Author];
Hermann, Andreas
[Author]
Chronic–Progressive Dopaminergic Deficiency Does Not Induce Midbrain Neurogenesis
You can manage bookmarks using lists, please log in to your user account for this.
Media type:
E-Article
Title:
Chronic–Progressive Dopaminergic Deficiency Does Not Induce Midbrain Neurogenesis
Contributor:
Fauser, Mareike
[Author];
Pan-Montojo, Francisco
[Author];
Richter, Christian
[Author];
Kahle, Philipp J.
[Author];
Schwarz, Sigrid C.
[Author];
Schwarz, Johannes
[Author];
Storch, Alexander
[Author];
Hermann, Andreas
[Author]
Footnote:
Hinweis: Link zur Erstveröffentlichung URL: https://doi.org/10.3390/cells10040775
Description:
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.