Treatment with Corticosterone Suppresses the Early Induction of MCP-1 After Neuronal Injury but Does Not Prevent Gliosis

Details

• Personal Author:
  Little AR ; O'Callaghan JP
• Description:
  Cytokines are proposed to play a role in central nervous system responses to injury and disease. One such response is neuronal damage-induced glial activation (gliosis). Here, we used the neurotoxic organometal, trimethyltin (TMT), to damage hippocampal pyramidal cells and elicit a glial response. In contrast to ischemic or traumatic brain injury models, TMT-induced neuronal damage is not associated with a compromised blood-brain barrier, nor is it associated with an inflammatory response, as evidenced by a lack of induction in TNF-alpha or IL-1B. Other chemokines and cytokines however, have been implicated in neural degeneration/regeneration responses and in the induction of gliosis. We confirmed the injury-associated expression of the chemokine monocyte chemoattractant protein (MCP)-1, in the TMT injury model and evaluated the effects of immune suppression on MCP-1 in relation to injury-induced gliosis. Induction of MCP-1 mRNA was assessed using semi-quantitative and quantitative RT-PCR (Taqman) at 2,5,& 8 hrs and 1,2,3,5,7 & 21 days after TMT (8 mg/kg, i.p.). Corticosterone (CORT) was administered in the drinking water (200 microg/ml). MCP-1 was elevated 100-fold 5 hours post TMT and increased until day 5. GFAP mRNA did not begin to increase until day 3, followed by an increase in GFAP (protein) at day 5. MCP-1 remained at control levels at all time points in the CORT/TMT group. These results demonstrate an involvement of MCP-1 in neural injury. MCP-1 and other inflammatory mediators do not appear to be required for glial activation because suppression of pro-inflammatory cytokines and chemokines by CORT does not alter the injury-induced glial response. [Description provided by NIOSH]
• Subjects:
  Animals Environmental Exposure Laboratories Nervous System Occupational Health Safety
• Keywords:
  Animal Studies Brain Damage Cellular Reactions Central Nervous System Central Nervous System Disorders Exposure Levels Laboratory Animals Models Neurological System Neurotoxic Effects Neurotoxins

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• ISSN:
  0190-5295
• Document Type:
  Text
• Genre:
  Abstract or Summary ; Proceedings
• Place as Subject:
  OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  26
• NIOSHTIC Number:
  nn:20020985
• Citation:
  Abstr - Soc Neurosci 2000 Nov; 26:1944
• Federal Fiscal Year:
  2001
• Peer Reviewed:
  False
• Source Full Name:
  Abstracts - Society for Neuroscience. Society for Neuroscience's 30th Annual Meeting, New Orleans, LA, November 4 - 9, 2000
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:26a5b8cf22daa71628d752e294aea4857f3a947126d62d36c0671f3180a200fc217d96e0dc714ffabf4a1de36397f370cedb1c83fc468b1093f523020026f0f2
• Download URL:
  https://stacks.cdc.gov/view/cdc/198588/cdc_198588_DS1.pdf
• File Type:
  [PDF - 29.07 KB ]