scholarly journals Withdrawal from Extended, Intermittent Access to A Highly Palatable Diet Impairs Hippocampal Memory Function and Neurogenesis: Effects of Memantine

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1520 ◽  
Author(s):  
Antonio Ferragud ◽  
Clara Velázquez-Sánchez ◽  
Ali Al Abdullatif ◽  
Valentina Sabino ◽  
Pietro Cottone
Keyword(s):  
Memory Function ◽  
Memory Deficits ◽  
Chow Group ◽  
Hippocampal Neurogenesis ◽  
Palatable Food ◽  
Hippocampal Function ◽  
Proliferating Cells ◽  
Intermittent Access ◽  
Male Wistar Rats ◽  
Palatable Diet

Background: Compulsive eating can be promoted by intermittent access to palatable food and is often accompanied by cognitive deficits and reduction in hippocampal plasticity. Here, we investigated the effects of intermittent access to palatable food on hippocampal function and neurogenesis. Methods: Male Wistar rats were either fed chow for 7 days/week (Chow/Chow group), or fed chow intermittently for 5 days/week followed by a palatable diet for 2 days/week (Chow/Palatable group). Hippocampal function and neurogenesis were assessed either during withdrawal or following renewed access to palatable food. Furthermore, the ability of the uncompetitive N-methyl-d-aspartate receptor (NMDAR) antagonist memantine to prevent the diet-induced memory deficits and block the maladaptive feeding was tested. Results: Palatable food withdrawn Chow/Palatable rats showed both a weakened ability for contextual spatial processing and a bias in their preference for a “novel cue” over a “novel place,” compared to controls. They also showed reduced expression of immature neurons in the dentate gyrus of the hippocampus as well as a withdrawal-dependent decrease of proliferating cells. Memantine treatment was able both to reverse the memory deficits and to reduce the excessive intake of palatable diet and the withdrawal-induced hypophagia in food cycling rats. Conclusions: In summary, our results provide evidence that withdrawal from highly palatable food produces NMDAR-dependent deficits in hippocampal function and a reduction in hippocampal neurogenesis.

scholarly journals Antiobesity Activity of Flavanoids Isolated from Solanum macrocarpum in Wistar Rats

2019 ◽  
pp. 1-9
Author(s):  
N. N. Ngwa ◽  
N. M. Nnam
Keyword(s):  
Total Cholesterol ◽  
Wistar Rats ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Triglyceride ◽  
Hdl Cholesterol ◽  
Chow Group ◽  
Male Wistar Rats ◽  
Palatable Diet ◽  
Acclimatization Period

Aims: To correlate obesity/atherosclerosis with body mass index, serum cholesterol, serum triglyceride, serum low density lipoprotein   and serum high density lipoprotein of diet induced obese wistar rats. Study Design: Department of Home Science, Nutrition and Dietetics (Animal research house) and Department of veterinary science both in University of Nigeria Nsukka. The study was conducted between January to March 2012. Methodology: Four groups of twenty male Wistar rats were fed a highly palatable diet for 2 weeks to induce obesity resembling mild obesity condition in human population after one week acclimatization period. DIO rats received rat chow and flavonoids extract daily for 6 weeks. Group 1 received rat chow alone; Group 2- 0.05% of flavonoids extract and rat chow; Group 3- 0.15% of flavonoid extract and rat chow; and Group 4- 0.25% of flavonoid extract and rat chow. BMI, Total cholesterol, HDL, LDL and Triglyceride were evaluated using standard assay technique. The data were statistically analyzed using ANOVA and mean separated using LSD. Results: Feeding the rats with palatable diet showed increased in BMI (from 0.35-0.40 to 0.60-0.65), total cholesterol, LDL and triglyceride levels along with decrease in HDL (p<0.05). Consumption of flavonoids resulted in the significant reduction in BMI, LDL, total cholesterol and triglyceride level and exhibit significant elevation in  HDL cholesterol compared to the rats fed only rat chow (p<0.05). It was observed that the decrease in BMI, Triglyceride, total  cholesterol and LDL cholesterol level of rats fed 0.25% of flavonoids were significantly different (p<0.05) from those fed 0.15% and 0.05% flavonoids. Conclusions: The results suggest that flavonoids extract from Solanum macranthum has atherogenic effect which can help to reduce obesity.

Investigating the effect of crocin on memory deficits induced by total sleep deprivation (TSD) with respect to the BDNF, TrkB and ERK levels in the hippocampus of male Wistar rats

2021 ◽  
pp. 026988112110007
Author(s):  
Malihe Looti Bashiyan ◽  
Mohammad Nasehi ◽  
Salar Vaseghi ◽  
Solmaz Khalifeh
Keyword(s):  
Sleep Deprivation ◽  
Memory Performance ◽  
Memory Function ◽  
Memory Deficits ◽  
Crocus Sativus ◽  
Protein Levels ◽  
Y Maze ◽  
Extracellular Signal ◽  
Improvement Effect ◽  
Male Wistar Rats

Background: Sleep deprivation (SD) induces cognitive impairments such as memory deficit. Brain-derived neurotrophic factor (BDNF) is considered as the most critical neurotrophin in the central nervous system that is involved in sleep and memory. The main receptor of BDNF, tropomyosin receptor kinase B (TrkB), is dramatically expressed in the hippocampus. Also, extracellular signal-regulated kinase (ERK) has a significant role in memory function. Crocin is a carotenoid chemical compound and the active component of the flower Crocus sativus L. (saffron) that improves memory function and increases the level of BDNF, TrkB and ERK. Aims: In this research, we aimed to investigate the effect of total SD (TSD, 24 h) and crocin on memory performance, and BDNF, TrkB and ERK hippocampal levels. Methods: Passive avoidance memory was assessed using step-through, and working memory was measured using Y-maze tasks. The level of proteins in both hemispheres of the hippocampus was evaluated using Western blotting. Crocin was injected intraperitoneally at doses of 1, 5 and 15 mg/kg. Results: Twenty-four-hour TSD impaired both types of memories and decreased the level of all proteins in both hemispheres of the hippocampus. Crocin at all doses restored TSD-induced memory deficits. Crocin (15 mg/kg) reversed the effect of TSD on levels of all proteins. Conclusions: The adverse effect of TSD on the level of proteins in the hippocampus may disrupt synaptic plasticity and transmission, which induces memory impairment. Additionally, the restoration effect of crocin on the decrease in protein levels may be involved in its improvement effect on memory performance.

scholarly journals Running throughout middle-age improves memory function, hippocampal neurogenesis, and BDNF levels in female C57BL/6J mice

2012 ◽  
Vol 72 (6) ◽  
pp. 943-952 ◽  
Author(s):  
Michael W. Marlatt ◽  
Michelle C. Potter ◽  
Paul J. Lucassen ◽  
Henriette van Praag
Keyword(s):  
Middle Age ◽  
Memory Function ◽  
Hippocampal Neurogenesis

Abstract P730: MCA Stroke Chronically Disrupts Hippocampal Activity and Cortico-Hippocampal Communication

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Zachary Ip ◽  
Gratianne Rabiller ◽  
Jiwei He ◽  
Shivalika Chavan ◽  
Yasuo Nishijima ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Memory Function ◽  
Brain Regions ◽  
Male Rats ◽  
Brain State ◽  
Signal Power ◽  
Hippocampal Function ◽  
Electrode Arrays ◽  
Mca Occlusion ◽  
Hippocampal Activity

Introduction: Cognition and memory deficits are common sequelae following middle cerebral artery (MCA) stroke, one of the most common strokes in humans. However MCA stroke does not compromise the structural integrity of the hippocampus, which is highly involved in memory function, because the MCA does not supply blood flow to the hippocampus. We previously reported on the acute effect of MCA stroke, where we observed increased hippocampal activity and cortico-hippocampal communication. Here we investigate chronic changes to local oscillations and cortico-hippocampal communication following MCA occlusion in rats two weeks and one month following stroke. Hypothesis: Cortical stroke affects remote brain regions, disrupting hippocampal function and cortico-hippocampal communication. Methods: We subjected male rats (n=28) to distal MCA occlusion compared to controls (n=19). We recorded local field potentials simultaneously from cortex and hippocampus two weeks and one month following stroke using 16-site linear electrode arrays under urethane anesthesia. We analyzed signal power, brain state, CFC, and sharp wave SPW-Rs to assess hippocampal function and cortico-hippocampal communication. Results: Our results show disruptions to local oscillations; lowered delta (1-3 Hz) signal power in the cortex and hippocampus, increased signal power in gamma (30-60 Hz) and high gamma (60-200 Hz) in cortex and hippocampus. Theta/delta brain state is disrupted, and SPW-Rs increase in power at two weeks, before returning to baseline levels at one month. Communication is also disrupted; Theta-gamma coupling, a measure of information being communicated between regions, breaks down after stroke. Conclusions: These results suggest that chronic stroke causes significant changes to hippocampal function, which can be characterized by these electrophysiological biomarkers, establishing putative targets for targeted stimulation therapies.

Abstract P783: Alpha 7 -Acetylcholine Receptor Signaling Reduces Neuronal Apoptosis After Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Ari Dienel ◽  
Remya A Veettil ◽  
Kanako Matsumura ◽  
Peeyush Kumar T. ◽  
Spiros Blackburn ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acetylcholine Receptor ◽  
Neuronal Apoptosis ◽  
Neuronal Survival ◽  
Memory Function ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory ◽  
Receptor Knockout Mouse

Subarachnoid hemorrhage induces neuronal apoptosis which causes acute and long-term memory deficits. Ourhypothesis is that agonism of α7-acetylcholine receptors attenuates neuronal apoptosis and improves memorydeficits in SAH mice. Mice were randomly assigned into the experimental groups. One cohort was euthanizedone day after SAH to assess neuronal apoptosis and signaling pathways. A second cohort survived for 30 dayspost-SAH to test long-term memory function. Inhibitors and an α7-acetylcholine receptor knockout mouse wereused. Neurobehavioral performance was assessed on days 1-3, 5, 7, and 23-28. All outcomes were performedand all data was analyzed by a blinded investigator. The α7-acetylcholine receptor agonist prevented neuronalapoptosis and improved acute memory deficits caused by SAH via activation of the PI3K/Akt pathway in neurons.Agonism of the α7-acetylcholine receptor was beneficial in both male and female mice, although the protectionin females was significantly better than in male mice. α7-acetylcholine receptor agonism did not provide anybenefit in α7-acetylcholine receptor knockout mice subjected to SAH. Treatment with the α7-acetylcholinereceptor agonist for 3 days after SAH led to improved working memory one month after SAH suggesting thatacutely improving neuronal survival can have long-lasting benefits. The α7-acetylcholine receptor may be atherapeutic target for SAH which can promote neuronal survival acutely after SAH, but also confer long-lastingmemory benefits. The findings of this study support the α7-acetylcholine receptor as a treatment target whichmay attenuate the long-term memory deficits which SAH patients suffer from.

scholarly journals Acute stress enhances adult rat hippocampal neurogenesis and activation of newborn neurons via secreted astrocytic FGF2

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Elizabeth D Kirby ◽  
Sandra E Muroy ◽  
Wayne G Sun ◽  
David Covarrubias ◽  
Megan J Leong ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Acute Stress ◽  
Memory Function ◽  
Brain Regions ◽  
Hippocampal Neurogenesis ◽  
Mammalian Brain ◽  
Stress Hormone ◽  
Adult Rat ◽  
Neural Stem Progenitor Cells ◽  
Newborn Neurons

Stress is a potent modulator of the mammalian brain. The highly conserved stress hormone response influences many brain regions, particularly the hippocampus, a region important for memory function. The effect of acute stress on the unique population of adult neural stem/progenitor cells (NPCs) that resides in the adult hippocampus is unclear. We found that acute stress increased hippocampal cell proliferation and astrocytic fibroblast growth factor 2 (FGF2) expression. The effect of acute stress occurred independent of basolateral amygdala neural input and was mimicked by treating isolated NPCs with conditioned media from corticosterone-treated primary astrocytes. Neutralization of FGF2 revealed that astrocyte-secreted FGF2 mediated stress-hormone-induced NPC proliferation. 2 weeks, but not 2 days, after acute stress, rats also showed enhanced fear extinction memory coincident with enhanced activation of newborn neurons. Our findings suggest a beneficial role for brief stress on the hippocampus and improve understanding of the adaptive capacity of the brain.

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