Spontaneous reactive astrogliosis in the dentate gyrus of bax-deficient mice

Research output: Contribution to journalArticle

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Abstract

Astrocytes play critical roles in many aspects of brain functions via modulation of neurotransmission, metabolism, and structural remodeling in response to physiological or pathological stimuli. Activation of astrocytes is a common phenomenon in many brain pathologies such as stroke, trauma, and neurodegenerative diseases. In this study, we found that gene deletion of the pro-apoptotic gene Bax (Bax-knockout) resulted in a spontaneous reactive astrogliosis in the dentate gyrus, as evidenced by the increased number/volume of astrocytes and cytoplasmic localization of the Olig2 protein. On the other hand, there was no evidence for microglial activation in the dentate gyrus of Bax-knockout mice. Previously, we reported that Bax-knockout mice failed to execute programmed cell death of adult-produced neurons, but the surplus neurons eventually impaired normal synaptic connections and dendritic arborization of dentate gyrus neurons. Therefore, we propose that the reactive astrocytes in the Baxknockout mice may play a role in tissue remodeling of the dentate gyrus following a failure in the programmed cell death of adult-produced neurons.

Original languageEnglish
Pages (from-to)379-383
Number of pages5
JournalMolecules and Cells
Volume31
Issue number4
DOIs
Publication statusPublished - 2011 Apr 1

Fingerprint

Dentate Gyrus
Astrocytes
Neurons
Knockout Mice
Cell Death
Neuronal Plasticity
Gene Deletion
Brain
Synaptic Transmission
Neurodegenerative Diseases
Stroke
Pathology
Wounds and Injuries
Genes
Proteins

Keywords

  • Astrogliosis
  • Bax
  • Microglial activation
  • Neurogenesis
  • Progrmmed cell death

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Spontaneous reactive astrogliosis in the dentate gyrus of bax-deficient mice. / Kim, Tae Woo; Kim, Hyun; Sun, Woong.

In: Molecules and Cells, Vol. 31, No. 4, 01.04.2011, p. 379-383.

Research output: Contribution to journalArticle

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