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Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Jones, K. A. (author)
Zouikr, I. (author)
Patience, M. (author)
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Clarkson, A. N. (author)
Isgaard, Jörgen, 1959 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition,Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Johnson, S. J. (author)
Spratt, N. (author)
Nilsson, M. (author)
Walker, F. R. (author)
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 (creator_code:org_t)
Elsevier BV, 2015
2015
English.
In: Brain Behavior and Immunity. - : Elsevier BV. - 0889-1591. ; 48, s. 57-67
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Post-stroke patients describe suffering from persistent and unremitting levels of distress. Using an experimental model of focal cortical ischemia in adult male C57BL/6 mice, we examined whether exposure to chronic stress could modify the development of secondary thalamic neurodegeneration (STND), which is commonly reported to be associated with impaired functional recovery. We were particularly focused on the modulatory role of microglia-like cells, as several clinical studies have linked microglial activation to the development of STND. One month following the induction of cortical ischemia we identified that numbers of microglial-like cells, as well as putative markers of microglial structural reorganization (Iba-1), complement processing (CD11b), phagocytosis (CD68), and antigen presentation (MHC-II) were all significantly elevated in response to occlusion. We further identified that these changes co-occurred with a decrease in the numbers of mature neurons within the thalamus. Occluded animals that were also exposed to chronic stress exhibited significantly lower levels of Iba-1 positive cells and a reduced expression of Iba-1 and CD11b compared to the 'occlusion-alone' group. Interestingly, the dampened expression of microglial/monocyte markers observed in stressed animals was associated with significant additional loss of neurons. These findings indicate that the process of STND can be negatively modified, potentially in a microglial dependent manner, by exposure to chronic stress. (C) 2015 Elsevier Inc. All rights reserved.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Immunology in the medical area (hsv//eng)

Keyword

Stroke
Chronic stress
Thalamus
Secondary neurodegeneration
Microglia
ANXIETY-LIKE BEHAVIOR
RECEPTOR ACTIVATION
CYTOKINE PRODUCTION
CEREBRAL-ISCHEMIA
PREFRONTAL CORTEX
DIFFUSION CHANGES
CORTICAL
STROKE
BRAIN-REGIONS
IN-VIVO
INFLAMMATION
Immunology
Neurosciences

Publication and Content Type

ref (subject category)
art (subject category)

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