Browsing by Subject "Spatial memory"

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    Chronic impairment of ERK signaling in glutamatergic neurons of the forebrain does not affect spatial memory retention and LTP in the same manner as acute blockade of the ERK pathway
    (Wiley, 2017-12) Vithayathil, Joseph; Pucilowska, Joanna; Friel, David; Landreth, Gary E.; Anatomy and Cell Biology, IU School of Medicine
    The ERK/MAPK signaling pathway has been extensively studied in the context of learning and memory. Defects in this pathway underlie genetic diseases associated with intellectual disability, including impaired learning and memory. Numerous studies have investigated the impact of acute ERK/MAPK inhibition on long-term potentiation and spatial memory. However, genetic knockouts of the ERKs have not been utilized to determine whether developmental perturbations of ERK/MAPK signaling affect LTP and memory formation in postnatal life. In this study, two different ERK2 conditional knockout mice were generated that restrict loss of ERK2 to excitatory neurons in the forebrain, but at different time-points (embryonically and post-natally). We found that embryonic loss of ERK2 had minimal effect on spatial memory retention and novel object recognition, while loss of ERK2 post-natally had more pronounced effects in these behaviors. Loss of ERK2 in both models showed intact LTP compared to control animals, while loss of both ERK1 and ERK2 impaired late phase LTP. These findings indicate that ERK2 is not necessary for LTP and spatial memory retention and provide new insights into the functional deficits associated with the chronic impairment of ERK signaling.
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    Coenzyme Q10 Prevents Scopolamine Associated Hippocampal-Dependent Memory Deficits in Mice
    (Elsevier, 2021) Kabir, Nadia; Pervin, Mst Shahnaj; Alam, Musrura Mefta; Mahmud, Waich; Zulfiker, Abu Hasanat Md.; Al Amin, Md. Mamun; Medical and Molecular Genetics, School of Medicine
    Scopolamine has been widely used to induce pharmacological model of memory impairment. Scopolamine impairs cognitive function via mitochondrial dysfunction and oxidative stress beyond that of direct cholinergic antagonism. Coenzyme Q10 (CoQ10), a mitochondrial component, protects mitochondria from reactive oxygen species and assist in energy production. Mitochondrial dysfunction appears with CoQ10 deficiency in the neurodegenerative disease. It is unknown whether CoQ10 can prevent scopolamine-associated spatial working memory deficits. We treated adult Swiss albino mice either by saline (control) or scopolamine or scopolamine plus CoQ10 or CoQ10 alone for four weeks and subsequently assessed spatial memory formation and locomotor activity. We euthanized mice to determine oxidative stress markers including lipid and protein oxidation, superoxide dismutase and catalase activity in brain tissues.Scopolamine-treated mice showed impaired spatial learning and memory formation. Scopolamine significantly increased levels of lipid peroxidation, reduced activity of superoxide dismutase and catalase compared to the controls. On the contrary, concomitant administration of scopolamine and CoQ10 did not cause spatial memory deficits. Furthermore, combined treatment did not alter hippocampal lipid and protein oxidation and activity of superoxide dismutase and catalase. Surprisingly, only CoQ10 supplementation improves oxidative stress markers compared to the control.Our results strongly suggest a protective ability of CoQ10 on spatial memory formation when concomitantly given with scopolamine in mice. The observed protective activity was presumably via an increased level of superoxide dismutase enzyme. We propose a further study to measure hippocampal mitochondrial function to reveal the underlying mechanism of CoQ10 before trial in humans.