Acute systemic heat stress increases glial fibrillary acidic protein immunoreactivity in brain: Experimental observations in conscious normotensive young rats

Sharma, H. S.; Zimmer, Claus; Westman, Jan; Cervós-Navarro, J.

doi:10.1016/0306-4522(92)90277-9

Cited by 94 publications

(54 citation statements)

References 55 publications

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“…3 to 5 mm thick) and embedded in paraffin. Approximately 3-μm thick sections were cut and stained with either Nissl, or hematoxylin and eosin (H&E) using standard techniques [51][52][53][54].…”

Section: Brain Pathologymentioning

confidence: 99%

Sleep Deprivation-Induced Blood-Brain Barrier Breakdown and Brain Dysfunction are Exacerbated by Size-Related Exposure to Ag and Cu Nanoparticles. Neuroprotective Effects of a 5-HT3 Receptor Antagonist Ondansetron

Sharma

Mureșanu²,

Lafuente

et al. 2015

Mol Neurobiol

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Military personnel are often subjected to sleep deprivation (SD) during combat operations. Since SD is a severe stress and alters neurochemical metabolism in the brain, a possibility exists that acute or long-term SD will influence blood-brain barrier (BBB) function and brain pathology. This hypothesis was examined in young adult rats (age 12 to 14 weeks) using an inverted flowerpot model. Rats were placed over an inverted flowerpot platform (6.5 cm diameter) in a water pool where the water levels are just 3 cm below the surface. In this model, animals can go to sleep for brief periods but cannot achieve deep sleep as they would fall into water and thus experience sleep interruption. These animals showed leakage of Evans blue in the cerebellum, hippocampus, caudate nucleus, parietal, temporal, occipital, cingulate cerebral cortices, and brain stem. The ventricular walls of the lateral and fourth ventricles were also stained blue, indicating disruption of the BBB and the blood-cerebrospinal fluid barrier (BCSFB). Breakdown of the BBB or the BCSFB fluid barrier was progressive in nature from 12 to 48 h but no apparent differences in BBB leakage were seen between 48 and 72 h of SD. Interestingly, rats treated with metal nanoparticles, e.g., Cu or Ag, showed profound exacerbation of BBB disruption by 1.5- to 4-fold, depending on the duration of SD. Measurement of plasma and brain serotonin showed a close correlation between BBB disruption and the amine level. Repeated treatment with the serotonin 5-HT3 receptor antagonist ondansetron (1 mg/kg, s.c.) 4 and 8 h after SD markedly reduced BBB disruption and brain pathology after 12 to 24 h SD but not following 48 or 72 h after SD. However, TiO2-nanowired ondansetron (1 mg/kg, s.c) in an identical manner induced neuroprotection in rats following 48 or 72 h SD. However, plasma and serotonin levels were not affected by ondansetron treatment. Taken together, our observations are the first to show that (i) SD could induce BBB disruption and brain pathology, (ii) nanoparticles exacerbate SD-induced brain damage, and (iii) serotonin 5-HT3 receptor antagonist ondansetron is neuroprotective in SD that is further potentiated byTiO2-nanowired delivery, not reported earlier.

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Section: Brain Pathologymentioning

confidence: 99%

Sleep Deprivation-Induced Blood-Brain Barrier Breakdown and Brain Dysfunction are Exacerbated by Size-Related Exposure to Ag and Cu Nanoparticles. Neuroprotective Effects of a 5-HT3 Receptor Antagonist Ondansetron

Sharma

Mureșanu²,

Lafuente

et al. 2015

Mol Neurobiol

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“…Bidirectional communication between the peripheral immune system and the CNS may be a mechanism by which resident brain cells are stimulated to produce cytokines, chemokines, and other inflammatory mediators of the SIRS symptoms (11). Glia are considered the main producers of cytokines and chemokines during peripheral inflammation (33) and may be operating similarly during HS (9,31). Yet, the association between glial reactivity, cytokine, and/or chemokine production in the brain and heat-induced SIRS responses has not been investigated.…”

mentioning

confidence: 99%

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Biedenkapp¹,

Leon

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Biedenkapp JC, Leon LR. Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery. Am J Physiol Regul Integr Comp Physiol 305: R978 -R986, 2013. First published September 11, 2013 doi:10.1152/ajpregu.00011.2013.-Heat stroke (HS) is characterized by a systemic inflammatory response syndrome (SIRS) consisting of profound core temperature (Tc) changes in mice. Encephalopathy is common at HS collapse, but inflammatory changes occurring in the brain during the SIRS remain unidentified. We determined the association between inflammatory gene expression changes in the brain with Tc disturbances during HS recovery in mice. Gene expression changes of heat shock protein (HSP)72, heme oxygenase (hmox1), cytokines (IL-1␤, IL-6, TNF-␣), cyclooxygenase enzymes (COX-1, COX-2), chemokines (MCP-1, MIP-1␣, MIP-1␤, CX 3CR1), and glia activation markers (CD14, aif1, vimentin) were examined in the hypothalamus (HY) and hippocampus (HC) of control (Tc ϳ 36.0°C) and HS mice at Tc,Max (42.7°C), hypothermia depth (HD; 29.3 Ϯ 0.4°C), and fever (37.8 Ϯ 0.3°C). HSP72 (HYϽHC) and IL-1␤ (HY only) were the only genes that showed increased expression at Tc,Max. HSP72 (HY Ͻ HC), hmox1 (HY Ͻ HC), cytokine (HY ϭ HC), and chemokine (HY ϭ HC) expression was highest at HD and similar to controls during fever. COX-1 expression was unaffected by HS, whereas HD was associated with approximately threefold increase in COX-2 expression (HY only). COX-2 expression was not increased during fever and indomethacin (COX inhibitor) had no effect on this Tc response indicating fever is regulated by other inflammatory pathways. CD14, aif1, and vimentin activation at HD coincided with maximal cytokine and chemokine expression suggesting glia cells are a possible source of brain cytokines and chemokines during HS recovery. The inflammatory gene expression changes during HS recovery suggest cytokines and/or chemokines may be initiating development or rewarming from hypothermia, whereas fever pathway(s) remain to be elucidated. heat stroke; cytokines; chemokines; hypothermia; fever; systemic inflammatory response HEAT STROKE (HS) is a serious form of hyperthermia characterized by a systemic inflammatory response syndrome (SIRS) leading to multiorgan dysfunction in which encephalopathy (e.g., ataxia, delirium, coma) predominates (5). The most common central nervous system (CNS) disturbance in HS patients is cerebellar dysfunction, which manifests as ataxia at the time of collapse (5,25,26). Postmortem analysis of HS victims showed histological damage and glia proliferation in the cerebellum that appeared to be the pathological basis for motor sequelae observed upon clinical admission (25). However, not all pathophysiological responses associated with the SIRS show a direct correlate to brain regions that experience cellular damage with HS. For example, HS patients and animal models often display core temperature (T c ) disturbances (e.g., hypothermia, fever) during recovery that occur in the absence of damage to the preoptic ante...

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“…However, the magnitude of heat induced glial cell reaction in different brain regions does not normally coincide with the severity of BBB breakdown or nerve cell injury. This indicates a selective difference in the vulnerability of neurons and glial cells in heat stress (Sharma et al, 1992d).…”

Section: Structural Changes In the Brain Following Heat Stressmentioning

confidence: 99%

Blood–Central Nervous System Barriers: The Gateway to Neurodegeneration, Neuroprotection and Neuroregeneration

Sharma¹

2009

Handbook of Neurochemistry and Molecular Neurobiology

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Acute systemic heat stress increases glial fibrillary acidic protein immunoreactivity in brain: Experimental observations in conscious normotensive young rats

Cited by 94 publications

References 55 publications

Sleep Deprivation-Induced Blood-Brain Barrier Breakdown and Brain Dysfunction are Exacerbated by Size-Related Exposure to Ag and Cu Nanoparticles. Neuroprotective Effects of a 5-HT3 Receptor Antagonist Ondansetron

Sleep Deprivation-Induced Blood-Brain Barrier Breakdown and Brain Dysfunction are Exacerbated by Size-Related Exposure to Ag and Cu Nanoparticles. Neuroprotective Effects of a 5-HT3 Receptor Antagonist Ondansetron

Increased cytokine and chemokine gene expression in the CNS of mice during heat stroke recovery

Blood–Central Nervous System Barriers: The Gateway to Neurodegeneration, Neuroprotection and Neuroregeneration

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