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Behav. Sci. 2018, 8(10), 93; https://doi.org/10.3390/bs8100093

Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats

1
Immunochemical Department, International Center for Neurological Restoration, 25th Ave, Playa, 15805, PC 11300 Havana, Cuba
2
Experimental Neurophysiology Department, International Center of Neurological Restoration (CIREN) Ave. 25 No. 15805 e/158 and 160, Playa, Havana 11300, Cuba
3
Physiologic Sciences Department, Latin American Medicine School, Carretera Panamericana, Kilómetro 3 1/2 Municipio Playa, Habana 19148, Cuba
*
Author to whom correspondence should be addressed.
Received: 22 August 2018 / Revised: 25 September 2018 / Accepted: 8 October 2018 / Published: 13 October 2018
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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. View Full-Text
Keywords: aging; learning; memory; neurotransmitter; oxidative stress; phospholipase A2; serine aging; learning; memory; neurotransmitter; oxidative stress; phospholipase A2; serine
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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González-Fraguela, M.E.; Blanco-Lezcano, L.; Fernandez-Verdecia, C.I.; Serrano Sanchez, T.; Robinson Agramonte, M.A.; Cardellá Rosales, L.L. Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats. Behav. Sci. 2018, 8, 93.

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