Architectural changes to CA1 pyramidal neurons in adult and aged mice after peripheral immune stimulation

Richwine, Amy F.; Parkin, Annie O.; Buchanan, Jessica B.; Chen, Jing; Markham, Julie A.; Juraska, Janice M.; Johnson, Rodney W.

doi:10.1016/j.psyneuen.2008.08.003

Cited by 80 publications

(76 citation statements)

References 39 publications

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“…Following LPS peripheral challenge, primed microglia were activated to a greater extent than MHC II-negative microglia and were highly responsible for the exaggerated production of IL-1b. These findings are in line with those of Richwine et al [111] who found higher steady-state expression of pro-inflammatory cytokines and decreased expression of neurotrophic factors in the hippocampus of aged mice compared with adults (Table 6). This was associated with increased vulnerability of CA1 neurons to LPS-induced neuroinflammation as shown by structural changes with decreased dendrite complexity compared to adult controls.…”

Section: Effects Of Acute Systemic Inflammation In the Ageing Brainsupporting

confidence: 92%

The neuroinflammatory hypothesis of delirium

et al. 2010

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Delirium is a neuropsychiatric syndrome characterized by a sudden and global impairment in consciousness, attention and cognition. It is particularly frequent in elderly subjects with medical or surgical conditions and is associated with short-and long-term adverse outcomes. The pathophysiology of delirium remains poorly understood as it involves complex multi-factorial dynamic interactions between a diversity of risk factors. Several conditions associated with delirium are characterized by activation of the inflammatory cascade with acute release of inflammatory mediators into the bloodstream. There is compelling evidence that acute peripheral inflammatory stimulation induces activation of brain parenchymal cells, expression of proinflammatory cytokines and inflammatory mediators in the central nervous system. These neuroinflammatory changes induce neuronal and synaptic dysfunction and subsequent neurobehavioural and cognitive symptoms. Furthermore, ageing and neurodegenerative disorders exaggerate microglial responses following stimulation by systemic immune stimuli such as peripheral inflammation and/or infection. In this review we explore the neuroinflammatory hypothesis of delirium based on recent evidence derived from animal and human studies.

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Section: Effects Of Acute Systemic Inflammation In the Ageing Brainsupporting

confidence: 92%

The neuroinflammatory hypothesis of delirium

et al. 2010

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“…The infection-induced hippocampal atrophy, which is mainly ascribed to the neurotoxic effects of immune challenge including inflammatory cytokine response, was reported. 21) Physical activity that is considered beneficial for mental health induces increased production of neurons, 22) while a lack of exercise impedes endogenous neurogenesis. 23) There were an increased number of apoptotic granular and pyramidal cells in the TUNEL assay and a decreased number of newborn cells on BrdU labeling in the hippocampus in our study.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Improves Hippocampal Atrophy in Chronic Fatigue Mice by Enhancing Neurogenesis and Inhibiting Apoptosis of Granular Cells

Moriya

Chen

Yamakawa

et al. 2011

Biological & Pharmaceutical Bulletin

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Chronic fatigue is reported in more than 20% of patients examined in primary care, and this common problem affects the quality of life and work productivity.1) A large part of the chronic fatigue population meets the diagnostic criteria for chronic fatigue syndrome (CFS), which is defined by unexplained physical or mental fatigue of at least 6-month duration and a combination of nonspecific symptoms.2) Several CFS symptoms including impaired concentration, attention, and memory as well as headache suggest that the central nervous system (CNS) may be involved in CFS pathophysiology.3) Moreover, neuroimaging evidence indicates that structural and/or functional abnormalities exist in the CNS of CFS patients. For example, marked reductions in the gray matter volume are observed; 4) Cook et al. 5) found an association between subjective feelings of mental fatigue and brain responses during a fatiguing cognitive task; CFS patients always have reduced concentrations of N-acetylaspartate in the hippocampus, a putative marker of neuronal metabolism 6) ; and a 23% reduction in 5-HT 1A receptor number and affinity was found in the hippocampus of CFS patients. 7) However, neural mechanisms, especially the hippocampal substrates in CFS, are unclear in part due to the lack of a suitable animal model.In our previous study, a chronic fatigue mouse model was induced by six repeated injections of fixed killed Brucella abortus antigen solution via the tail vein every 2 weeks. 8,9) We found that brain atrophy and reduction of the hippocampal Bcl-2 and brain-derived neurotrophic factor (BDNF) mRNA expression levels were accompanied by lower spontaneous activity.8) However, the hippocampal weight was not measured in those previous studies.Resveratrol (RSV), an active component of grapevines and peanuts, is recognized as a polyphenolic activator of sirtuin 1 (Sirt1), a protein deacetylase.10) It can enhance running activity of high fat diet-fed mice two-fold by activating Sirt1. 11)Moreover, Sirt1 can protect neurons from DNA damageinduced apoptosis by downregulating p53 acetylation, an apoptotic mediator.12) RSV treatment of neural progenitor cells (NPCs) is capable of increasing differentiation and directing neurogenesis through a mechanism requiring Sirt1.13) Thus RSV may be beneficial for physical activity of our fatigue mice and even play a role in improving structural and/or functional defects of the hippocampus.We aimed to clarify the hippocampal structural and/or functional defects in this fatigue model. Another purpose of our study was to determine whether RSV intervention could improve the fatigue and reverse the abnormalities by antiapoptosis and promoting neurogenesis. MATERIALS AND METHODS Animals, Living Conditions, and Spontaneous RunningActivity Eight-week old BALB/c mice (female, 20-24 g, CLEA Japan, Tokyo, Japan) were housed singly in previously described cages 8,9) including running wheels and counters. The cages were maintained under a light-dark photoperiod (lights on from 09:00 to 17:00), and daily spontaneous ...

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“…In several situations of enhanced innate immunity, such as in lipopolysaccharide-challenged mice, IL6 plays an essential role in alterations of hippocampal biochemistry, structure, and functions (Dantzer et al ., 1999;Goshen et al ., 2007;Richwine et al ., 2008). In the IL15 ligand and receptor KO mice, however, serum IL6 remained low.…”

Section: Discussionmentioning

confidence: 99%

Essential role of interleukin-15 receptor in normal anxiety behavior

Hsuchou

et al. 2010

Brain, Behavior, and Immunity

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The interactions between the cytokine interleukin (IL)-15 and the classical neurotransmitter GABA have been shown in IL15Rα receptor knockout mice by observations of memory deficits and reduction of GABA. To test the hypothesis that IL15 affects anxiety-like behavior, knockout mice without IL15, IL15Rα, or the co-receptor IL2Rγ were subjected to open-field and elevated plus maze tests. All three strains showed reduction of anxiety, with greater changes in the IL15Rα knockout mice than in the IL15 or IL2Rγ knockout mice. This unexpected observation is opposite to the reported increase of anxiety in mice lacking other proinflammatory cytokines or their receptors. The reduced anxiety was not associated with changes in associated serum cytokines. However, western blotting, qPCR, and immunohistochemistry all showed that IL15Rα knockout mice had mild microgliosis and astrogliosis in the hippocampus. To determine whether this gliosis plays a role in decreasing anxiety, IL15Rα knockout mice were treated with minocycline, but this did not cause a change in open field performance. To determine whether IL15 plays a direct role in anxiety, wildtype mice were treated with IL15 by intraperitoneal injection. This also failed to cause a change in open field behavior under the experimental conditions tested. Thus, IL15Rα is essential for normal anxietylike behavior, but inhibition of gliosis in the fearless IL15Rα knockout mice or IL15 treatment of normal mice did not acutely modulate behavioral performance as tested.

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Architectural changes to CA1 pyramidal neurons in adult and aged mice after peripheral immune stimulation

Cited by 80 publications

References 39 publications

The neuroinflammatory hypothesis of delirium

The neuroinflammatory hypothesis of delirium

Resveratrol Improves Hippocampal Atrophy in Chronic Fatigue Mice by Enhancing Neurogenesis and Inhibiting Apoptosis of Granular Cells

Essential role of interleukin-15 receptor in normal anxiety behavior

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