10.3389/fcell.2019.00158.s001
Teresa Muro-García
Teresa
Muro-García
Soraya Martín-Suárez
Soraya
Martín-Suárez
Nelson Espinosa
Nelson
Espinosa
Roberto Valcárcel-Martín
Roberto
Valcárcel-Martín
Ainhoa Marinas
Ainhoa
Marinas
Laura Zaldumbide
Laura
Zaldumbide
Lara Galbarriatu
Lara
Galbarriatu
Amanda Sierra
Amanda
Sierra
Pablo Fuentealba
Pablo
Fuentealba
Juan Manuel Encinas
Juan Manuel
Encinas
Data_Sheet_1_Reactive Disruption of the Hippocampal Neurogenic Niche After Induction of Seizures by Injection of Kainic Acid in the Amygdala.docx
Frontiers
2019
neural stem cells
hippocampal neurogenesis
seizures
gliosis
amygdala
2019-08-20 12:14:30
Dataset
https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_Reactive_Disruption_of_the_Hippocampal_Neurogenic_Niche_After_Induction_of_Seizures_by_Injection_of_Kainic_Acid_in_the_Amygdala_docx/9692492
<p>Adult neurogenesis persists in the adult hippocampus due to the presence of multipotent neural stem cells (NSCs). Hippocampal neurogenesis is involved in a range of cognitive functions and is tightly regulated by neuronal activity. NSCs respond promptly to physiological and pathological stimuli altering their neurogenic and gliogenic potential. In a mouse model of mesial temporal lobe epilepsy (MTLE), seizures triggered by the intrahippocampal injection of the glutamate receptor agonist kainic acid (KA) induce NSCs to convert into reactive NSCs (React-NSCs) which stop producing new neurons and ultimately generate reactive astrocytes thus contributing to the development of hippocampal sclerosis and abolishing neurogenesis. We herein show how seizures triggered by the injection of KA in the amygdala, an alternative model of MTLE which allows parallel experimental manipulation in the dentate gyrus, also trigger the induction of React-NSCs and provoke the disruption of the neurogenic niche resulting in impaired neurogenesis. These results highlight the sensitivity of NSCs to the surrounding neuronal circuit activity and demonstrate that the induction of React-NSCs and the disruption of the neurogenic niche are not due to the direct effect of KA in the hippocampus. These results also suggest that neurogenesis might be lost in the hippocampus of patients with MTLE. Indeed we provide results from human MTLE samples absence of cell proliferation, of neural stem cell-like cells and of neurogenesis.</p>