scholarly journals Calbindin-1 Expression in the Hippocampus following Neonatal Hypoxia-Ischemia and Therapeutic Hypothermia and Deficits in Spatial Memory

2018 ◽  
Vol 40 (5-6) ◽  
pp. 508-522 ◽  
Author(s):  
Janasha Goffigan-Holmes ◽  
Dafne Sanabria ◽  
Johana Diaz ◽  
Debra Flock ◽  
Raul Chavez-Valdez
Keyword(s):  
Therapeutic Hypothermia ◽  
Neurodegenerative Disorders ◽  
Memory Impairment ◽  
Memory Deficits ◽  
Nissl Staining ◽  
Memory Impairments ◽  
Neonatal Hypoxia ◽  
Y Maze ◽  
Hypoxia Ischemia ◽  
With Memory

Hippocampal injury following neonatal hypoxia-ischemia (HI) leads to memory impairments despite therapeutic hypothermia (TH). In the hippocampus, the expression of calbindin-1 (Calb1), a Ca2+-buffering protein, increases during postnatal development and decreases with aging and neurodegenerative disorders. Since persistent Ca2+ dysregulation after HI may lead to ongoing injury, persistent changes in hippocampal expression of Calb1 may contribute to memory impairments after neonatal HI. We hypothesized that, despite TH, neonatal HI persistently decreases Calb1 expression in the hippocampus, a change associated with memory deficits in the mouse. We induced cerebral HI in C57BL6 mice at postnatal day 10 (P10) with right carotid ligation and 45 min of hypoxia (FiO2 = 0.08), followed by normothermia (36°C, NT) or TH (31°C) for 4 h with anesthesia-shams as controls. Nissl staining and glial fibrillary acidic protein (GFAP) immunohistochemistry (IHC) were used to grade brain injury and astrogliosis at P11, P18, and P40 prior to the assessment of Calb1 expression by IHC. The subset of mice followed to P40 also performed a memory behavior task (Y-maze) at P22–P26. Nonparametric statistics stratified by sex were applied. In both anterior and posterior coronal brain sections, hippocampal Calb1 expression doubled between P11 and P40 due to an increase in the cornus ammonis (CA) field (Kruskal-Wallis [KW] p < 0.001) and not the dentate gyrus (DG). Neonatal HI produced delayed (P18) and late (P40) deficits in the expression of Calb1 exclusively in the CA field (KW p = 0.02) in posterior brain sections. TH did not attenuate Calb1 deficits after HI. Thirty days after HI injury (at P40), GFAP scores in the hippocampus (p < 0.001, r = –0.47) and CA field (p < 0.001, r = –0.39) of posterior brain sections inversely correlated with their respective Calb1 expression. Both sexes demonstrated deficits in Y-maze testing, including approximately 40% lower spontaneous alterations performance and twice as much total impairment compared to sham mice (KW p < 0.001), but it was only in females that these deficits correlated with the Calb1 expression in the hippocampal CA field (p < 0.05) of the posterior sections. Hippocampal atrophy after neonatal HI also correlated with worse deficits in Y-maze testing, but it did not predict Calb1 deficits. Neonatal HI produces a long-lasting Calb1 deficit in the hippocampal CA field during development, which is not mitigated by TH. Late Calb1 deficit after HI may be the result of persistent astrogliosis and can lead to memory impairment, particularly in female mice.

scholarly journals Effect of Metformin on Doxorubicin-Induced Memory Dysfunction

2020 ◽  
Vol 10 (3) ◽  
pp. 152
Author(s):  
Ibrahim Alharbi ◽  
Hindi Alharbi ◽  
Yasser Almogbel ◽  
Abdullah Alalwan ◽  
Ahmad Alhowail
Keyword(s):  
Cognitive Dysfunction ◽  
Memory Impairment ◽  
Elevated Plus Maze ◽  
Male Rats ◽  
Memory Impairments ◽  
Glucose Levels ◽  
Y Maze ◽  
Altered Glucose ◽  
Plus Maze ◽  
With Memory

Doxorubicin (DOX) is widely used to treat many types of cancer; however, it is associated with chemotherapy-related complications such as cognitive dysfunction, known as chemobrain. Chemobrain affects up to 75% of cancer survivors, and there are currently no available therapeutic options. This study aims to examine whether metformin (MET) can protect against the neurotoxicity caused by DOX treatment. Forty male rats were divided into four groups (10 rats/group): control, DOX, DOX + MET, and MET. Rats treated with DOX received five doses of 4 mg/kg DOX weekly (cumulative dose: 20 mg/kg). For the DOX-MET and MET groups, MET (3 mg/mL) was dissolved in drinking water. Behavioral and glucose tests were performed one day after treatment was completed. We found DOX (4 mg/kg/week, 5 weeks) caused learning and memory impairment in the Y-maze, novel object recognition, and elevated plus maze behavioral tests. MET did not rescue these DOX-induced memory impairments. Neither DOX nor MET nor MET + DOX altered glucose levels following the treatment. In summary, DOX treatment is associated with memory impairment in rats, but MET does not rescue this cognitive dysfunction.

scholarly journals Ursolic acid attenuates beta-amyloid-induced memory impairment in mice

2016 ◽  
Vol 74 (6) ◽  
pp. 482-488 ◽  
Author(s):  
Wenna Liang ◽  
Xiaoyang Zhao ◽  
Jinping Feng ◽  
Fenghua Song ◽  
Yunzhi Pan
Keyword(s):  
Oxidative Stress ◽  
Ursolic Acid ◽  
Memory Impairment ◽  
Tumor Necrosis ◽  
Therapeutic Strategy ◽  
Antioxidant Activities ◽  
Neuroprotective Effect ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Memory Impairments

ABSTRACT Objective Increasing evidence demonstrates that oxidative stress and inflammatory are involved in amyloid β (Aβ)-induced memory impairments. Ursolic acid (UA), a triterpenoid compound, has potent anti-inflammatory and antioxidant activities. However, it remains unclear whether UA attenuates Aβ-induced neurotoxicity. Method The aggregated Aβ25-35 was intracerebroventricularly administered to mice. Results We found that UA significantly reversed the Aβ25-35-induced learning and memory deficits. Our results indicated that one of the potential mechanisms of the neuroprotective effect was attenuating the Aβ25-35-induced accumulation of malondialdehyde (MDA) and depletion of glutathione (GSH) in the hippocampus. Furthermore, UA significantly suppressed the upregulation of IL-1β, IL-6, and tumor necrosis-α factor levels in the hippocampus of Aβ25-35-treated mice. Conclusion These findings suggest that UA prevents memory impairment through amelioration of oxidative stress, inflammatory response and may offer a novel therapeutic strategy for the treatment of Alzheimer’s disease.

Early enriched housing results in partial recovery of memory deficits in female, but not in male, rats after neonatal hypoxia–ischemia

2008 ◽  
Vol 1218 ◽  
pp. 257-266 ◽  
Author(s):  
Lenir Orlandi Pereira ◽  
Atahualpa Cauê Paim Strapasson ◽  
Patrícia Machado Nabinger ◽  
Matilde Achaval ◽  
Carlos Alexandre Netto
Keyword(s):  
Memory Deficits ◽  
Male Rats ◽  
Partial Recovery ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
Recovery Of Memory

Effects of daily environmental enrichment on memory deficits and brain injury following neonatal hypoxia-ischemia in the rat

2007 ◽  
Vol 87 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Lenir Orlandi Pereira ◽  
Nice Sarmento Arteni ◽  
Ruth Chamorro Petersen ◽  
Anderson Padilha da Rocha ◽  
Matilde Achaval ◽  
...  
Keyword(s):  
Brain Injury ◽  
Environmental Enrichment ◽  
Memory Deficits ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Delayed injury of hippocampal interneurons after neonatal hypoxia-ischemia and therapeutic hypothermia in a murine model

Hippocampus ◽  
2018 ◽  
Vol 28 (8) ◽  
pp. 617-630 ◽  
Author(s):  
Raul Chavez-Valdez ◽  
Paul Emerson ◽  
Janasha Goffigan-Holmes ◽  
Alfredo Kirkwood ◽  
Lee J. Martin ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Murine Model ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Effects of therapeutic hypothermia on white matter injury from murine neonatal hypoxia–ischemia

2017 ◽  
Vol 82 (3) ◽  
pp. 518-526 ◽  
Author(s):  
Elliot Koo ◽  
R Ann Sheldon ◽  
Byong Sop Lee ◽  
Zinaida S Vexler ◽  
Donna M Ferriero
Keyword(s):  
White Matter ◽  
Therapeutic Hypothermia ◽  
White Matter Injury ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Schizandrin, an Antioxidant Lignan fromSchisandra chinensis,Ameliorates Aβ1–42-Induced Memory Impairment in Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Di Hu ◽  
Yunfeng Cao ◽  
Rongrong He ◽  
Na Han ◽  
Zhihui Liu ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Water Maze ◽  
Memory Impairment ◽  
Reference Memory ◽  
Reference Drug ◽  
Memory Impairments ◽  
Maze Test ◽  
Y Maze ◽  
Spatial Reference Memory ◽  
Antioxidative Enzyme Activities

In the present study, we examined the effect of schisandrin (SCH) ofSchisandra chinensison the amyloid-beta1–42- (Aβ1–42-) induced memory impairment in mice and elucidated the possible antioxidative mechanism. Mice were intracerebroventricular (i.c.v.) injected with the aggregated Aβ1–42and then treated with SCH (4, 12, and 36 mg/kg body weight) or donepezil (DPZ), a reference drug (0.65 mg/kg) by intragastric infusion for 14 days. Noncognitive disturbances and cognitive performance were evaluated by locomotor activity test, Y-maze test, and water maze test. Antioxidative enzyme activities including superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and levels of malondialdehyde (MDA), glutathione (GSH), and oxidized glutathione (GSSG) within the cerebral cortex and hippocampus of mice were measured to elucidate the mechanism. Our results showed that SCH significantly improved Aβ1–42-induced short-term and spatial reference memory impairments in Y-maze test and water maze test. Furthermore, in the cerebral cortex and hippocampus of mice, SOD and GSH-px activities, GSH level, and GSH/GSSG ratio were increased, and levels of MDA and GSSG were decreased by the treatment of SCH. These results suggest that SCH is a potential cognitive enhancer against Alzheimer’s disease through antioxidative action.

scholarly journals Early Hippocampal Sharp-Wave Ripple Deficits Predict Later Learning and Memory Impairments in an Alzheimer’s Disease Mouse Model

2019 ◽  
Author(s):  
Emily A. Jones ◽  
Anna K. Gillespie ◽  
Seo Yeon Yoon ◽  
Loren M. Frank ◽  
Yadong Huang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Genetic Risk ◽  
Memory Impairment ◽  
Memory Loss ◽  
Memory Deficits ◽  
Power Reduction ◽  
Memory Impairments ◽  
Sharp Wave

SUMMARYAlzheimer’s disease (AD) is characterized by progressive memory loss, and there is a pressing need to identify early pathophysiological alterations that predict subsequent memory impairment. Hippocampal sharp-wave ripples (SWRs) – electrophysiological signatures of memory reactivation in the hippocampus – are a compelling candidate for doing so. Mouse models of AD show reductions in both SWR abundance and associated slow gamma (SG) power during aging, but these alterations have yet to be directly linked to memory impairments. In aged apolipoprotein E4 knock in (apoE4-KI) mice – a model of the major genetic risk factor for AD – we found that reduced SWR abundance and associated CA3 SG power predicted spatial memory impairments measured 1–2 months later. Importantly, SWR-associated CA3 SG power reduction in young apoE4-KI mice also predicted spatial memory deficits measured 10 months later. These results establish features of SWRs as potential functional biomarkers of memory impairment in AD.

BDNF Protects against Spatial Memory Deficits Following Neonatal Hypoxia-Ischemia

2000 ◽  
Vol 166 (1) ◽  
pp. 99-114 ◽  
Author(s):  
C.Robert Almli ◽  
Todd J. Levy ◽  
Byung Hee Han ◽  
Aarti R. Shah ◽  
Jeffrey M. Gidday ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Memory Deficits ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia
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