Ageing is accompanied by a decline in cognitive functions; along with a variety of neurobiological changes. The association between inflammation and ageing is based on complex molecular and cellular changes that we are only just beginning to understand. The hippocampus is one of the structures more closely related to electrophysiological, structural and morphological changes during ageing. In the present study we examined the effect of normal ageing and LPS-induced inflammation on astroglia-neuron interaction in the rat hippocampus of adult, normal aged and LPS-treated adult rats. Astrocytes were smaller, with thicker and shorter branches and less numerous in CA1 Str. radiatum of aged rats in comparison to adult and LPS-treated rats. Astrocyte branches infiltrated apoptotic neurons of aged and LPS-treated rats. Cellular debris, which were more numerous in CA1 of aged and LPS-treated rats, could be found apposed to astrocytes processes and were phagocytated by reactive microglia. Reactive microglia were present in the CA1 Str. Radiatum, often in association with apoptotic cells. Significant differences were found in the fraction of reactive microglia which was 40% of total in adult, 33% in aged and 50% in LPS-treated rats. Fractalkine (CX3CL1) increased significantly in hippocampus homogenates of aged and LPS-treated rats. The number of CA1 neurons decreased in aged rats. In the hippocampus of aged and LPS-treated rats astrocytes and microglia may help clearing apoptotic cellular debris possibly through CX3CL1 signalling. Our results indicate that astrocytes and microglia in the hippocampus of aged and LPS-infused rats possibly participate in the clearance of cellular debris associated with programmed cell death. The actions of astrocytes may represent either protective mechanisms to control inflammatory processes and the spread of further cellular damage to neighboring tissue, or they may contribute to neuronal damage in pathological conditions.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3445467PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0045250PLOS

Publication Analysis

Top Keywords

lps-treated rats
24
aged lps-treated
20
cellular debris
12
reactive microglia
12
rats
10
aged
9
rat hippocampus
8
rats astrocytes
8
numerous ca1
8
ca1 str
8

Similar Publications

Saccharomyces boulardii Ameliorates LPS-Induced Amyloidogenesis in Rats.

Probiotics Antimicrob Proteins

December 2024

Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, P.O. Box, Tehran, 19839-63113, Iran.

Gut brain axis can affect the incidence of Alzheimer's disease (AD). Probiotics restore the homeostasis of gut dysbiosis and prevent AD. Here, we evaluated the impact of Saccharomyces boulardii on rats with lipopolysaccharide (LPS)-induced amyloidogenesis.

View Article and Find Full Text PDF

KAT3B-mediated succinylation of DERL3 suppresses osteogenic differentiation by promoting M1/M2 macrophage polarization.

Biochem Pharmacol

December 2024

Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontics, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai 200072, China.

Periodontitis is a chronic inflammatory disease influenced by macrophage polarization. Additionally, succinylation-enriched Porphyromonas gingivalis is a pathogenic factor of periodontitis. However, the role of succinylation in the pathogenesis of periodontitis remains unclear.

View Article and Find Full Text PDF

Spinal AT1R contributes to neuroinflammation and neuropathic pain via NOX2-dependent redox signaling in microglia.

Free Radic Biol Med

December 2024

Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, China. Electronic address:

Microglia-mediated neuroinflammation demonstrates a crucial act in the progression of neuropathic pain. Oxidative damage induced by reactive oxygen species (ROS) derived from NADPH oxidase (NOX) in microglia drives proinflammatory microglia activation. Recent evidence points to the central renin angiotensin system (RAS) is involved in oxidative stress and neuroinflammation, with the angiotensin converting enzyme/angiotensin II/angiotensin receptor-1 (ACE/Ang II/AT1R) axis promoting inflammation through increased ROS production, counteracted by the ACE2/Ang (1-7)/Mas receptor (MasR) axis.

View Article and Find Full Text PDF

Brain inflammation and oxidative stress play critical roles in neuronal apoptosis and memory dysfunction in Alzheimer's disease. Crocin, a natural carotenoid in the stigma of saffron, possesses radical scavenging, anti-inflammatory, and anti-apoptotic properties. This study investigates the protective impact of crocin on neuronal apoptosis, oxidative stress, neuroinflammation, and memory deficits induced by lipopolysaccharide (LPS) in rats.

View Article and Find Full Text PDF

Background: Oxycodone, a widely used opioid analgesic, has an unbound brain-to-plasma concentration ratio (K) greater than unity, indicating active uptake across brain barriers associated with the putative proton-coupled organic cation (H/OC) antiporter system. With this study, we aimed to elucidate oxycodone's CNS disposition during lipopolysaccharide (LPS)-induced systemic inflammation in Sprague-Dawley rats.

Methods: Using brain microdialysis, we dynamically and simultaneously monitored unbound oxycodone concentrations in blood, striatum, lateral ventricle, and cisterna magna following intravenous administration of oxycodone post-LPS challenge.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!