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Updated: Feb 3, 2026

Cellular Redox Profiling Using High-content Microscopy
Published on: May 14, 2017
Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats
Maria Elena González-Fraguela1, Lisette Blanco-Lezcano2, Caridad Ivette Fernandez-Verdecia3
1Immunochemical Department, International Center for Neurological Restoration, 25th Ave, Playa, 15805, PC 11300 Havana, Cuba. marie@neuro.ciren.cu.
Abstract:
The purpose of the present study is to access the linkage between dysregulation of glutamatergic neurotransmission, oxidative metabolism, and serine signaling in age-related cognitive decline. In this work, we evaluated the effect of natural aging in rats on the cognitive abilities for hippocampal-dependent tasks. Oxidative metabolism indicators are glutathione (GSH), malondialdehyde (MDA) concentrations, and cytosolic phospholipase A₂ (PLA₂) activity. In addition, neurotransmitter amino acid (L-Glutamic acid, γ-aminobutyric acid (GABA), DL-Serine and DL-Aspartic acid) concentrations were studied in brain areas such as the frontal cortex (FC) and hippocampus (HPC). The spatial long-term memory revealed significant differences among experimental groups: the aged rats showed an increase in escape latency to the platform associated with a reduction of crossings and spent less time on the target quadrant than young rats. Glutathione levels decreased for analyzed brain areas linked with a significant increase in MDA concentrations and PLA₂ activity in cognitive-deficient old rats. We found glutamate levels only increased in the HPC, whereas a reduced level of serine was found in both regions of interest in cognitive-deficient old rats. We demonstrated that age-related changes in redox metabolism contributed with alterations in synaptic signaling and cognitive impairment.
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