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Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
Published on: November 14, 2013
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Diazepam Inhibits Post-Traumatic Neurogenesis and Blocks Aberrant Dendritic Development
Laura E Villasana1, Austin Peters1, Raluca McCallum2
11Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Journal of Neurotrauma
|February 23, 2019
Summary
The benzodiazepine diazepam (DZP) prevents the increase in new hippocampal neurons and their abnormal growth after traumatic brain injury (TBI) in mice. Further research is needed to understand DZP's effects on TBI recovery.
Area of Science:
- Neuroscience
- Cell Biology
- Trauma Research
Background:
- Traumatic brain injury (TBI) increases hippocampal neurogenesis, but new neurons mature abnormally.
- Gamma-aminobutyric acid A receptors (GABAARs) influence neuronal growth.
- Sedatives targeting GABAARs are used in TBI patients.
Purpose of the Study:
- To investigate if diazepam (DZP), a benzodiazepine, affects neurogenesis after TBI.
- To determine DZP's impact on the maturation of newly formed neurons in the hippocampus.
Main Methods:
- Adult mice underwent controlled cortical impact (CCI) TBI.
- DZP or vehicle was administered for one week post-injury via osmotic pump.
- Neurogenesis, dendritic outgrowth, cortical injury, reactive gliosis, cell proliferation, and c-Fos activation were assessed.
Main Results:
- DZP did not affect neurogenesis in control mice.
- DZP nearly abolished the TBI-induced increase in hippocampal neurogenesis.
- DZP prevented aberrant dendritic growth of post-TBI neurons and reduced c-Fos activation.
Conclusions:
- Diazepam significantly inhibits TBI-induced hippocampal neurogenesis and abnormal neuronal development.
- The findings suggest a link between neuronal activity and post-injury neurogenesis.
- Further studies are essential to evaluate benzodiazepine effects on cognitive recovery and complications following TBI.
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