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Combined Mechanical and Enzymatic Dissociation of Mouse Brain Hippocampal Tissue
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Hippocampal structure and function are maintained despite severe innate peripheral inflammation.

Patrick Süß1, Liubov Kalinichenko2, Wolfgang Baum3

  • 1Department of Molecular Neurology, Friedrich-Alexander-University Erlangen-Nürnberg, University Hospital Erlangen, Schwabachanlage 6, 91054 Erlangen, Germany.

Brain, Behavior, and Immunity
|June 16, 2015
PubMed
Summary

Severe peripheral inflammation in rheumatoid arthritis models does not trigger depression or affect the hippocampus. This suggests the brain maintains immunity and plasticity despite systemic inflammation, challenging links between peripheral cytokines and depressive behavior.

Keywords:
Adult hippocampal neurogenesisAnxietyDepressionLocomotionNeuroinflammationPeripheral inflammation

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Area of Science:

  • Neuroimmunology
  • Rheumatology
  • Psychiatry

Background:

  • Chronic peripheral inflammation, involving cytokines like TNFα, IL-1β, and IL-6, is linked to depression and anxiety.
  • The specific peripheral inflammatory triggers for neuroinflammation and subsequent depressive behavior remain unclear.

Purpose of the Study:

  • To investigate if chronic peripheral inflammation in TNF-α transgenic (TNFtg) mice, a model for rheumatoid arthritis, induces neuroinflammation and depressive-like behavior.
  • To examine the impact on adult hippocampal neurogenesis and plasticity.

Main Methods:

  • Utilized the human TNF-α transgenic (TNFtg) mouse model exhibiting rheumatoid arthritis.
  • Assessed inflammatory markers (IL-1β, IL-6, TNF-α) in serum, joints, and hippocampus.
  • Evaluated hippocampal microgliosis, astrocytosis, locomotion, and adult hippocampal neurogenesis.

Main Results:

  • TNFtg mice displayed severe erosive arthritis with elevated peripheral inflammatory markers.
  • Hippocampal IL-1β and IL-6 mRNA levels were unchanged, and signs of neuroinflammation were absent.
  • Locomotion was impaired, but no depression-like behavior was observed; hippocampal neurogenesis remained intact.

Conclusions:

  • Peripheral inflammation in TNFtg mice, driven by innate immune system activation, does not directly cause depressive-like behavior or neuroinflammation.
  • The hippocampus maintains its immunity, cellular plasticity, and function despite significant peripheral inflammation.
  • Findings challenge the direct causal link between severe peripheral inflammation and depression-mediated behavioral changes.