ArticlePloS one2017
A noradrenergic lesion aggravates the effects of systemic inflammation on the hippocampus of aged rats.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- The Effect of Disulfiram and N-Acetylcysteine, Potential Compensators for Sulfur Disorders, on Lipopolysaccharide-Induced Neuroinflammation Leading to Memory Impairment and the Metabolism of L-Cysteine Disturbance.Molecules (Basel, Switzerland) · 2025Article
- Monoamine signaling and neuroinflammation: mechanistic connections and implications for neuropsychiatric disorders.Frontiers in immunology · 2025Review
- MM165 - A Small Hybrid Molecule Modulates the Kynurenine Pathway and Attenuates Lipopolysaccharide-Induced Memory Deficits and Inflammation.Neurochemical research · 2024Article
- Locus coeruleus injury modulates ventral midbrain neuroinflammation during DSS-induced colitis.Research square · 2024Article
- Influence of Mild Chronic Stress and Social Isolation on Acute Ozone-Induced Alterations in Stress Biomarkers and Brain-Region-Specific Gene Expression in Male Wistar-Kyoto Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Inhibition of rat locus coeruleus neurons by prostaglandin EFrontiers in pharmacology · 2023Article
- Dexmedetomidine Ameliorated Cognitive Dysfunction Induced by Intestinal Ischemia Reperfusion in Mice with Possible Relation to the Anti-inflammatory Effect Through the Locus Coeruleus Norepinephrine System.Neurochemical research · 2022Article
- Inflaming the Brain with Iron.Antioxidants (Basel, Switzerland) · 2021Review
- Curiosity-Based Interventions Increase Everyday Functioning Score But Not Serum BDNF Levels in a Cohort of Healthy Older Adults.Frontiers in aging · 2021Article
- Locus Coeruleus Modulates Neuroinflammation in Parkinsonism and Dementia.International journal of molecular sciences · 2020Review
- Transgenic Mice Expressing Human α-Synuclein in Noradrenergic Neurons Develop Locus Ceruleus Pathology and Nonmotor Features of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Stress and brain immunity: Microglial homeostasis through hypothalamus-pituitary-adrenal gland axis and sympathetic nervous system.Brain, behavior, & immunity - health · 2020Review
- Neuroinflammation in Aged Brain: Impact of the Oral Administration of Ellagic Acid Microdispersion.International journal of molecular sciences · 2020Article
- Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer's disease.Neurobiology of aging · 2020Article
- The Noradrenergic System in Parkinson's Disease.Frontiers in pharmacology · 2020Review
- Stress-induced microglial activation occurs through β-adrenergic receptor: noradrenaline as a key neurotransmitter in microglial activation.Journal of neuroinflammation · 2019Article
- The contribution of the locus coeruleus-norepinephrine system in the emergence of defeat-induced inflammatory priming.Brain, behavior, and immunity · 2019Article
- The Neuroprotective Effects of Exercise: Maintaining a Healthy Brain Throughout Aging.Brain plasticity (Amsterdam, Netherlands) · 2018Review
- α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson's Disease Pathogenesis.Frontiers in neuroscience · 2018Review
- Noradrenergic Hypothesis Linking Neurodegeneration-Based Cognitive Decline and Astroglia.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroinflammation is potentiated by early degeneration of the locus coeruleus noradrenergic pathway (LC-NE) commonly seen in aging-related neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In animal models, lipopolysaccharide (LPS) induces strong peripheral immune responses that can cause cognitive changes secondary to neuroinflammation. The influence of the peripheral immune response on cognition might be exacerbated by LC-NE degeneration, but this has not been well characterized previously. In this study, we investigated how systemic inflammation affects neuroinflammation and cognition in aged rats that have had either normal or damaged LC-NE transmitter systems. Rats were first exposed to the selective noradrenergic (NE) neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) to induce degeneration of central NE pathways. Two weeks later, the rats received a low dose of LPS. This resulted in 3 treatment groups (Control, LPS-, and DSP4+LPS-treated rats) studied at 4 hours (short-term subgroup) and 7 days (long-term subgroup) following the LPS injection. DSP4+LPS-treated rats exhibited increased serum levels of several pro-inflammatory cytokines, increased astroglial and microglial activation in the hippocampus, and poorer performance in the novel object recognition task (NORT) compared to controls and LPS-treated rats. Additionally, serum and brain tissue levels of brain-derived neurotrophic factor (BDNF) were modulated over time in the DSP4+LPS group compared to the other two groups. Specifically, DSP4+LPS-treated rats in the short-term subgroup had lower hippocampal BDNF levels (~25%) than controls and LPS-treated rats, which negatively correlated with hippocampal astrogliosis and positively correlated with hippocampal IL-1β levels. Serum and hippocampal BDNF levels in the DSP4+LPS-treated rats in the long-term subgroup returned to levels similar to the control group. These results show that systemic inflammation in LC-NE-lesioned aged rats promotes an exacerbated systemic and central inflammatory response compared to LC-NE-intact rats and alters BDNF levels, indicating the important role of this neurotransmitter system in response to neuroinflammation.
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