scholarly journals New hippocampal neurons are not obligatory for memory formation; cyclin D2 knockout mice with no adult brain neurogenesis show learning

2009 ◽  
Vol 16 (7) ◽  
pp. 439-451 ◽  
Author(s):  
P. Jaholkowski ◽  
A. Kiryk ◽  
P. Jedynak ◽  
N. M. Ben Abdallah ◽  
E. Knapska ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Hippocampal Neurons ◽  
Memory Formation ◽  
Adult Brain ◽  
Cyclin D2

scholarly journals Impaired Generation of Transit-Amplifying Progenitors in the Adult Subventricular Zone of Cyclin D2 Knockout Mice

Cells ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 135
Author(s):  
Rafał Płatek ◽  
Piotr Rogujski ◽  
Jarosław Mazuryk ◽  
Marta B. Wiśniewska ◽  
Leszek Kaczmarek ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Hippocampal Neurons ◽  
Adult Brain ◽  
Cyclin D2 ◽  
Olfactory Bulbs ◽  
Differentiation Potential ◽  
Neural Precursors ◽  
Neurogenic Niche ◽  
Regenerative Therapies

In the adult brain, new neurons are constitutively derived from postnatal neural stem cells/progenitors located in two neurogenic regions: the subventricular zone (SVZ) of the lateral ventricles (migrating and differentiating into different subtypes of the inhibitory interneurons of the olfactory bulbs), and the subgranular layer of the hippocampal dentate gyrus. Cyclin D2 knockout (cD2-KO) mice exhibit reduced numbers of new hippocampal neurons; however, the proliferation deficiency and the dysregulation of adult neurogenesis in the SVZ required further investigation. In this report, we characterized the differentiation potential of each subpopulation of the SVZ neural precursors in cD2-KO mice. The number of newly generated cells in the SVZs was significantly decreased in cD2-KO mice compared to wild type mice (WT), and was not accompanied by elevated levels of apoptosis. Although the number of B1-type quiescent precursors (B1q) and the overall B1-type activated precursors (B1a) were not affected in the SVZ neurogenic niche, the number of transit-amplifying progenitors (TaPs) was significantly reduced. Additionally, the subpopulations of calbindin D28k and calretinin interneurons were diminished in the olfactory bulbs of cD2-KO mice. Our results suggest that cyclin D2 might be critical for the proliferation of neural precursors and progenitors in the SVZ—the transition of B1a into TaPs and, thereafter, the production of newly generated interneurons in the olfactory bulbs. Untangling regulators that functionally modulate adult neurogenesis provides a basis for the development of regenerative therapies for injuries and neurodegenerative diseases.

scholarly journals Circuit Integration Initiation of New Hippocampal Neurons in the Adult Brain

Cell Reports ◽  
2020 ◽  
Vol 30 (4) ◽  
pp. 959-968.e3 ◽  
Author(s):  
Chih-Hao Yang ◽  
Adrian Di Antonio ◽  
Gregory W. Kirschen ◽  
Parul Varma ◽  
Jenny Hsieh ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Adult Brain ◽  
Circuit Integration

scholarly journals Increased ethanol intake and preference in cyclin D2 knockout mice

2011 ◽  
Vol 10 (5) ◽  
pp. 551-556 ◽  
Author(s):  
P. Jaholkowski ◽  
P. Mierzejewski ◽  
P. Zatorski ◽  
A. Scinska ◽  
H. Sienkiewicz-Jarosz ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Ethanol Intake ◽  
Cyclin D2

scholarly journals Lack of cyclin D2 impairing adult brain neurogenesis alters hippocampal-dependent behavioral tasks without reducing learning ability

2012 ◽  
Vol 227 (1) ◽  
pp. 159-166 ◽  
Author(s):  
Paulina Jedynak ◽  
Piotr Jaholkowski ◽  
Grazyna Wozniak ◽  
Carmen Sandi ◽  
Leszek Kaczmarek ◽  
...  
Keyword(s):  
Adult Brain ◽  
Learning Ability ◽  
Cyclin D2 ◽  
Behavioral Tasks

scholarly journals Telomerase increasing compound protects hippocampal neurons from amyloid beta toxicity by enhancing the expression of neurotrophins and plasticity related genes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Natalie Baruch-Eliyahu ◽  
Vladislav Rud ◽  
Alex Braiman ◽  
Esther Priel
Keyword(s):  
Oxidative Stress ◽  
Amyloid Beta ◽  
Neurotrophic Factors ◽  
Hippocampal Neurons ◽  
Neuroprotective Effect ◽  
Adult Brain ◽  
Beta Catenin ◽  
Adult Mice ◽  
Hippocampal Cell Culture ◽  
Neuronal Degradation

AbstractThe telomerase reverse transcriptase protein, TERT, is expressed in the adult brain and its exogenic expression protects neurons from oxidative stress and from the cytotoxicity of amyloid beta (Aβ). We previously showed that telomerase increasing compounds (AGS) protected neurons from oxidative stress. Therefore, we suggest that increasing TERT by AGS may protect neurons from the Aβ-induced neurotoxicity by influencing genes and factors that participate in neuronal survival and plasticity. Here we used a primary hippocampal cell culture exposed to aggregated Aβ and hippocampi from adult mice. AGS treatment transiently increased TERT gene expression in hippocampal primary cell cultures in the presence or absence of Aβ and protected neurons from Aβ induced neuronal degradation. An increase in the expression of Growth associated protein 43 (GAP43), and Feminizing locus on X-3 genes (NeuN), in the presence or absence of Aβ, and Synaptophysin (SYP) in the presence of Aβ was observed. GAP43, NeuN, SYP, Neurotrophic factors (NGF, BDNF), beta-catenin and cyclin-D1 expression were increased in the hippocampus of AGS treated mice. This data suggests that increasing TERT by pharmaceutical compounds partially exerts its neuroprotective effect by enhancing the expression of neurotrophic factors and neuronal plasticity genes in a mechanism that involved Wnt/beta-catenin pathway.

scholarly journals Cacna1c: Protecting young hippocampal neurons in the adult brain

Neurogenesis ◽  
2016 ◽  
Vol 3 (1) ◽  
pp. e1231160 ◽  
Author(s):  
Héctor De Jesús-Cortés ◽  
Anjali M. Rajadhyaksha ◽  
Andrew A. Pieper
Keyword(s):  
Hippocampal Neurons ◽  
Adult Brain

Memory formation and retention are affected in adult miR-132/212 knockout mice

2015 ◽  
Vol 287 ◽  
pp. 15-26 ◽  
Author(s):  
Julia Hernandez-Rapp ◽  
Pascal Y. Smith ◽  
Mohammed Filali ◽  
Claudia Goupil ◽  
Emmanuel Planel ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Memory Formation

scholarly journals Cloning and Characterization of Rat Caspase-9: Implications for a Role in Mediating Caspase-3 Activation and Hippocampal Cell Death after Transient Cerebral Ischemia

2002 ◽  
Vol 22 (5) ◽  
pp. 534-546 ◽  
Author(s):  
Guodong Cao ◽  
Yumin Luo ◽  
Tetsuya Nagayama ◽  
Wei Pei ◽  
R. Anne Stetler ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Neuronal Survival ◽  
Global Ischemia ◽  
Adult Brain ◽  
Caspase 8 ◽  
Intrinsic Pathway ◽  
Caspase 9 ◽  
Transient Global Ischemia

Delayed hippocampal neurodegeneration after transient global ischemia is mediated, at least in part, through the activation of terminal caspases, particularly caspase-3, and the subsequent proteolytic degradation of critical cellular proteins. Caspase-3 may be activated by the membrane receptor-initiated caspase-8–dependent extrinsic pathway and the mitochondria-initiated caspase-9–dependent intrinsic pathway; however, the precise role of these deduced apoptosis-signaling pathways in activating caspase-3 in ischemic neurons remains elusive. The authors cloned the caspase-9 gene from the rat brain and investigated its potential role in mediating ischemic neuronal death in a rat model of transient global ischemia. Caspase-9 gene expression and protease activity were extremely low in the adult brain, whereas they were developmentally upregulated in newborn rats, especially at postnatal 12 weeks, a finding consistent with the theory of an essential role for caspase-9 in neuronal apoptosis during brain development. After 15-minute transient global ischemia, caspase-9 was overexpressed and proteolytically activated in the hippocampal CA1 neurons at 8 to 72 hours of reperfusion. The temporal profile of caspase-9 activation coincided with that of cytochrome c release and caspase-3 activation, but preceded CA1 neuronal death. Immunoprecipitation experiments revealed that there was enhanced formation of Apaf-1/caspase-9 complex in the hippocampus 8 and 24 hours after ischemia. Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3–like activity and significantly enhanced neuronal survival in the CA1 sector. In contrast, inhibition of caspase-8 activity had no significant effect on caspase-3 activation or neuronal survival. These results suggest that the caspase-9–dependent intrinsic pathway may be the primary mechanism responsible for the activation of caspase-3 in ischemic hippocampal neurons.

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