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J Neuroimmunol. 2017 Aug 20. pii: S0165-5728(17)30204-7. doi: 10.1016/j.jneuroim.2017.08.008. [Epub ahead of print]

Absence of the neurogenesis-dependent nuclear receptor TLX induces inflammation in the hippocampus.

Author information

1
Department of Anatomy and Neuroscience, University College Cork, Ireland.
2
Department of Anatomy, National University of Ireland, Galway, Ireland.
3
Department of Anatomy and Neuroscience, University College Cork, Ireland; APC Microbiome Institute, University College Cork, Ireland.
4
Department of Anatomy and Neuroscience, University College Cork, Ireland; APC Microbiome Institute, University College Cork, Ireland. Electronic address: y.nolan@ucc.ie.

Abstract

The orphan nuclear receptor TLX (Nr2e1) is a key regulator of hippocampal neurogenesis. Impaired adult hippocampal neurogenesis has been reported in neurodegenerative and psychiatric conditions including dementia and stress-related depression. Neuroinflammation is also implicated in the neuropathology of these disorders, and has been shown to negatively affect hippocampal neurogenesis. To investigate a role for TLX in hippocampal neuroinflammation, we assessed microglial activation in the hippocampus of mice with a spontaneous deletion of TLX. Results from our study suggest that a lack of TLX is implicated in deregulation of microglial phenotype and that consequently, the survival and function of newborn cells in the hippocampus is impaired. TLX may be an important target in understanding inflammatory-associated impairments in neurogenesis.

KEYWORDS:

DCX; Hippocampus; Interleukin-1β; Microglia; Neurogenesis; TLX

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