scholarly journals Time-dependent roles of adolescent- and adult-born dentate granule neurons in spatial learning

2020 ◽  
Author(s):  
Nuria Masachs ◽  
Vanessa Charrier ◽  
Fanny Farrugia ◽  
Valerie Lemaire ◽  
Wilfrid Mazier ◽  
...  

SUMMARYThe dentate gyrus presents the peculiarity to be formed after birth in rodents. Adolescence is a very sensitive period during which cognitive competences are programmed. We investigated and compared the role of dentate neurons born during adolescence or generated during adulthood. We demonstrated that the ontogenetic stage of dentate neurons in relation to when they are generated dictates their participation in memory processes.

Author(s):  
Nuria Masachs ◽  
Vanessa Charrier ◽  
Fanny Farrugia ◽  
Valerie Lemaire ◽  
Nicolas Blin ◽  
...  

AbstractThe dentate gyrus is one of the only brain regions that continues its development after birth in rodents. Adolescence is a very sensitive period during which cognitive competences are programmed. We investigated the role of dentate granule neurons (DGNs) born during adolescence in spatial memory and compared them with those generated earlier in life (in embryos or neonates) or during adulthood by combining functional imaging, retroviral and optogenetic tools to tag and silence DGNs. By imaging DGNs expressing Zif268, a proxy for neuronal activity, we found that neurons generated in adolescent rats (and not embryos or neonates) are transiently involved in spatial memory processing. In contrast, adult-generated DGNs are recruited at a later time point when animals are older. A causal relationship between the temporal origin of DGNs and spatial memory was confirmed by silencing DGNs in behaving animals. Our results demonstrate that the emergence of spatial memory depends on neurons born during adolescence, a function later assumed by neurons generated during adulthood.


2009 ◽  
Vol 42 (05) ◽  
Author(s):  
Y Golub ◽  
CP Mauch ◽  
F Pamplona ◽  
CT Wotjak

2007 ◽  
Author(s):  
Emily Kern ◽  
David H. Uttal ◽  
Natalya Murashev ◽  
Linda Liu Hand
Keyword(s):  

2017 ◽  
Vol 313 (5) ◽  
pp. L899-L915 ◽  
Author(s):  
Fumiaki Kato ◽  
Seiichiro Sakao ◽  
Takao Takeuchi ◽  
Toshio Suzuki ◽  
Rintaro Nishimura ◽  
...  

Pulmonary arterial hypertension (PAH) is characterized by progressive obstructive remodeling of pulmonary arteries. However, no reports have described the causative role of the autophagic pathway in pulmonary vascular endothelial cell (EC) alterations associated with PAH. This study investigated the time-dependent role of the autophagic pathway in pulmonary vascular ECs and pulmonary vascular EC kinesis in a severe PAH rat model (Sugen/hypoxia rat) and evaluated whether timely induction of the autophagic pathway by rapamycin improves PAH. Hemodynamic and histological examinations as well as flow cytometry of pulmonary vascular EC-related autophagic pathways and pulmonary vascular EC kinetics in lung cell suspensions were performed. The time-dependent and therapeutic effects of rapamycin on the autophagic pathway were also assessed. Sugen/hypoxia rats treated with the vascular endothelial growth factor receptor blocker SU5416 showed increased right ventricular systolic pressure (RVSP) and numbers of obstructive vessels due to increased pulmonary vascular remodeling. The expression of the autophagic marker LC3 in ECs also changed in a time-dependent manner, in parallel with proliferation and apoptotic markers as assessed by flow cytometry. These results suggest the presence of cross talk between pulmonary vascular remodeling and the autophagic pathway, especially in small vascular lesions. Moreover, treatment of Sugen/hypoxia rats with rapamycin after SU5416 injection activated the autophagic pathway and improved the balance between cell proliferation and apoptosis in pulmonary vascular ECs to reduce RVSP and pulmonary vascular remodeling. These results suggested that the autophagic pathway can suppress PAH progression and that rapamycin-dependent activation of the autophagic pathway could ameliorate PAH.


1995 ◽  
Vol 31 (5) ◽  
pp. 379-409 ◽  
Author(s):  
Edward R. Hirt ◽  
Hugh E. McDonald ◽  
Grant A. Erickson

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