Ruth M. Barrientos

ORCID: 0000-0001-7224-4109
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Stress Responses and Cortisol
  • Tryptophan and brain disorders
  • Immune Response and Inflammation
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroscience and Neuropharmacology Research
  • Cancer, Stress, Anesthesia, and Immune Response
  • Intensive Care Unit Cognitive Disorders
  • Anesthesia and Neurotoxicity Research
  • Diet and metabolism studies
  • Memory and Neural Mechanisms
  • Immune cells in cancer
  • Fatty Acid Research and Health
  • Alzheimer's disease research and treatments
  • Adipokines, Inflammation, and Metabolic Diseases
  • Neuroendocrine regulation and behavior
  • Regulation of Appetite and Obesity
  • Circadian rhythm and melatonin
  • Nerve injury and regeneration
  • Neuropeptides and Animal Physiology
  • Neurological Disease Mechanisms and Treatments
  • Gut microbiota and health
  • Dietary Effects on Health
  • Long-Term Effects of COVID-19
  • MicroRNA in disease regulation

Institute for Behavioral Medicine
2018-2025

The Ohio State University
2018-2025

Johns Hopkins Medicine
2023

Johns Hopkins University
2023

University of California, Irvine
2023

Mayo Clinic
2023

The Ohio State University Wexner Medical Center
2019-2020

University of Colorado Boulder
2011-2020

University of Colorado System
2016-2018

Medizinische Hochschule Hannover
2008

To investigate the role of pro-inflammatory cytokine interleukin-1β (IL-1β) in postoperative cognitive dysfunction (POCD) aged rats, we used laparotomy to mimic human abdominal surgery adult (3 months) and (24 F344/BN rats. We demonstrated that memory consolidation hippocampal-dependent contextual fear-conditioning task is significantly impaired but not young rats 4 d after surgery. Hippocampal-independent auditory-cued fear was disrupted by either age group. The impairment paralleled...

10.1523/jneurosci.2173-12.2012 article EN cc-by-nc-sa Journal of Neuroscience 2012-10-17

It is argued that the hippocampus contributes to contextual fear conditioning by supporting acquisition of a conjunctive memory representation context, which associates with shock. This function was examined studying context pre-exposure facilitation effect (CPFE). A rat shocked immediately after being placed into subsequently displays almost no context. However, if it pre-exposed day before immediate shock, significant freezing By using 5-aminomethyl-3-hydroxysoxazole temporarily inactivate...

10.1523/jneurosci.1598-03.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-03-10

It has been proposed that contextual fear conditioning depends on 2 processes: (a) construction of a conjunctive representation the features make up context and (b) association with shock. Support for this view comes from studies indicating prior exposure to facilitates supported by immediate Thus, produced shock is memory preexposed context, which activated retrieval cues associated context. The authors' experiments support interpretation indicate process an intact hippocampal formation....

10.1037//0735-7044.116.4.530 article EN Behavioral Neuroscience 2002-01-01

We have previously found that healthy aged rats are more likely to suffer profound memory impairments following a severe bacterial infection than younger adult rats. Such peripheral challenge is capable of producing neuroinflammatory response, and in the brain this response exaggerated prolonged. Normal aging primes, or sensitizes, microglia, appears be source amplified inflammatory response. Among outcomes synaptic plasticity reductions brain-derived neurotrophic factor (BDNF), both which...

10.1523/jneurosci.2266-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-08-10

Amplified neuroinflammatory responses following an immune challenge occur with normal aging and can elicit or exacerbate neuropathology. The mechanisms mediating this sensitized "primed" response in the aged brain are not fully understood. alarmin high mobility group box 1 (HMGB1) be released under chronic pathological conditions initiate inflammatory cascades. This led us to investigate whether HMGB1 regulates age-related priming of response. Here, we show that protein mRNA were elevated...

10.1523/jneurosci.1161-16.2016 article EN Journal of Neuroscience 2016-07-27

For reasons that are not well understood, aging significantly increases brain vulnerability to challenging life events. High-functioning older individuals often experience significant cognitive decline after an inflammatory event such as surgery, infection, or injury. We have modeled this phenomenon in rodents and previously reported a peripheral immune challenge (intraperitoneal injection of live Escherichia coli ) selectively disrupts consolidation hippocampus-dependent memory aged...

10.1523/jneurosci.5818-10.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-03-16

Glia are now recognized as important contributors in pathological pain creation and maintenance. Spinal cord glia exhibit extensive gap junctional connectivity, raising the possibility that involved contralateral spread of excitation resulting mirror image pain. In present experiments, junction decoupler carbenoxolone was administered intrathecally after induction neuropathic response to sciatic nerve inflammation (sciatic inflammatory neuropathy) or partial injury (chronic constriction...

10.1016/j.jpain.2004.06.006 article EN publisher-specific-oa Journal of Pain 2004-09-01
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