scholarly journals Subregion-specific p300 conditional knock-out mice exhibit long-term memory impairments

2011 ◽  
Vol 18 (3) ◽  
pp. 161-169 ◽  
Author(s):  
A. M. M. Oliveira ◽  
M. A. Estevez ◽  
J. D. Hawk ◽  
S. Grimes ◽  
P. K. Brindle ◽  
...  
Keyword(s):  
Long Term Memory ◽  
Term Memory ◽  
Knock Out ◽  
Memory Impairments ◽  
Knock Out Mice

scholarly journals Cyclin D2-knock-out mice with attenuated dentate gyrus neurogenesis have robust deficits in long-term memory formation

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Stela P. Petkova ◽  
Michael Pride ◽  
Carolyn Klocke ◽  
Timothy A. Fenton ◽  
Jeannine White ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Memory Formation ◽  
Long Term Memory ◽  
Cyclin D2 ◽  
Term Memory ◽  
Knock Out ◽  
Knock Out Mice

scholarly journals Hyperfunction of Muscarinic Receptor Maintains Long-Term Memory in 5-HT4 Receptor Knock-Out Mice

PLoS ONE ◽  
2010 ◽  
Vol 5 (3) ◽  
pp. e9529 ◽  
Author(s):  
Luis Segu ◽  
Marie-José Lecomte ◽  
Mathieu Wolff ◽  
Julie Santamaria ◽  
René Hen ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Long Term Memory ◽  
Term Memory ◽  
Knock Out ◽  
Knock Out Mice

scholarly journals Spatial learning and long-term memory impairments in RasGrf1 KO, Pttg1 KO, and double KO mice

2018 ◽  
Vol 8 (11) ◽  
pp. e01089 ◽  
Author(s):  
Lara Manyes ◽  
Sarah Holst ◽  
Manuel Lozano ◽  
Eugenio Santos ◽  
Alberto Fernandez-Medarde
Keyword(s):  
Spatial Learning ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Impairments

Silymarin Prevents Memory Impairments, Anxiety, and Depressive-Like Symptoms in a Rat Model of Post-Traumatic Stress Disorder

Planta Medica ◽  
2018 ◽  
Vol 85 (01) ◽  
pp. 32-40 ◽  
Author(s):  
Tamam El-Elimat ◽  
Karem Alzoubi ◽  
Mahmoud AbuAlSamen ◽  
Zeinab Al Subeh ◽  
Tyler Graf ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Anxiety And Depression ◽  
Long Term Memory ◽  
Post Traumatic Stress ◽  
Term Memory ◽  
Memory Impairments ◽  
Post Traumatic

AbstractPost-traumatic stress disorder (PTSD) is a debilitating psychopathological disease that is triggered by exposure to traumatic events. It is usually associated with substantial comorbidities, such as cognitive impairment, anxiety, and depression. Silymarin has been recently reported to exert neuroprotective activities against neurodegenerative diseases such as Alzheimerʼs and Parkinsonʼs diseases. Herein, the beneficial effects of silymarin in ameliorating PTSD-like symptoms such as memory impairments, anxiety, and depression were evaluated using a single-prolonged stress (SPS) rat model of PTSD. Male Wistar rats were randomly assigned into four groups: control, silymarin, SPS, or SPS + silymarin. Rats were administrated silymarin, 100 mg/kg i. p. for 4 wk. Rats in all groups were tested for short- and long-term memory in the radial arm water maze (RAWM), for anxiety-like behaviors using the open field test (OFT) and elevated plus maze (EPM) test, and for depression-like symptoms using the tail suspension test (TST). Conventional analyses of the RAWM, EPM, OFT, and TST were conducted using analysis of variance. Additionally, the anxiety-related behavior parameters of the EPM and OFT were entered to principal component analysis. Regression scores based on the first two extracted components, which accounted for 61% of the variance, were indicative of the anxiolytic activity of silymarin. Collectively, the results suggest that silymarin treatment prevents SPS-induced long-term memory impairments, anxiety, and depressive-like symptoms in rat models.

scholarly journals Disturbance in Mammalian Cognition Caused by Accumulation of Silver in Brain

Toxics ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 30 ◽  
Author(s):  
Anna A. Antsiferova ◽  
Marina Yu. Kopaeva ◽  
Vyacheslav N. Kochkin ◽  
Pavel K. Kashkarov ◽  
Mikhail V. Kovalchuk
Keyword(s):  
Silver Nanoparticles ◽  
Long Term Memory ◽  
Cell Integrity ◽  
Prolonged Administration ◽  
Term Memory ◽  
Histological Studies ◽  
Memory Impairments ◽  
Hippocampal Cell ◽  
The Brain

The influence of daily prolonged administration of silver nanoparticles on the cognitive functions of a model mammal was studied. The accumulation of silver in the whole brain and the hippocampus, cerebellum, cortex and residual brain tissue of the mouse was investigated by highly precise and representative neutron activation analysis, and histological studies were conducted. Here, we show that long-term memory impairments were caused by the accumulation of silver nanoparticles in the brain and its subregions, such as the hippocampus, cerebellum and cortex, in a step-like manner by disturbance of hippocampal cell integrity. Three different approaches allowed us to observe this phenomenon and discover the reasons it occurred.

scholarly journals Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein

2010 ◽  
Vol 107 (5) ◽  
pp. 2295-2300 ◽  
Author(s):  
Claudia Balducci ◽  
Marten Beeg ◽  
Matteo Stravalaci ◽  
Antonio Bastone ◽  
Alessandra Sclip ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Prion Protein ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Long Term Memory ◽  
Ample Evidence ◽  
Knock Out ◽  
Intracerebroventricular Injections ◽  
Knock Out Mice

Inability to form new memories is an early clinical sign of Alzheimer’s disease (AD). There is ample evidence that the amyloid-β (Aβ) peptide plays a key role in the pathogenesis of this disorder. Soluble, bio-derived oligomers of Aβ are proposed as the key mediators of synaptic and cognitive dysfunction, but more tractable models of Aβ−mediated cognitive impairment are needed. Here we report that, in mice, acute intracerebroventricular injections of synthetic Aβ1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ1–42 fibrils and freshly dissolved peptide did not. The deficit induced by oligomers was reversible and was prevented by an anti-Aβ antibody. It has been suggested that the cellular prion protein (PrPC) mediates the impairment of synaptic plasticity induced by Aβ. We confirmed that Aβ1–42 oligomers interact with PrPC, with nanomolar affinity. However, PrP-expressing and PrP knock-out mice were equally susceptible to this impairment. These data suggest that Aβ1–42 oligomers are responsible for cognitive impairment in AD and that PrPC is not required.

scholarly journals Memory impairments and increased GFAP expression in hippocampal astrocytes following hypercaloric diet in rats

2019 ◽  
Vol 77 (9) ◽  
pp. 601-608 ◽  
Author(s):  
Eduardo Fernandes Bondan ◽  
Carolina Vieira Cardoso ◽  
Maria de Fátima Monteiro Martins ◽  
Rosemari Otton
Keyword(s):  
Adipose Tissue ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Memory Impairments ◽  
Tissue Weight ◽  
Adipose Tissue Weight ◽  
Brown Adipose ◽  
Hypercaloric Diet

ABSTRACT Objective: Hypothalamic inflammation and glial fibrillary acidic protein (GFAP) overexpression in astrocytes are well described in obese animals, as are some cognitive and memory deficits. As the hippocampus plays important roles in the consolidation of information, this investigation aimed to observe the memory function and the astrocyte expression of GFAP in the hippocampus of rats that received either a hypercaloric or a normocaloric diet. Methods: Adult male Wistar rats received a high-fat (cafeteria) or a standard diet for 60 days. On the 61st day, the rats were submitted to the novel object recognition (NOR) test at three and 24 hours after the first contact with objects, to assess short-term and long-term memory, respectively. Thereafter, the rats were euthanized and their brains were collected for GFAP immunohistochemical investigation in the hippocampus (CA1, CA2, CA3 areas) and hypothalamus (periventricular and arcuate nuclei). Astrocytic reactivity was assessed by morphometry. Different white adipose tissue depots and brown adipose tissue were weighed to calculate the adiposity index. Results: The hypercaloric diet increased body weight gain, adiposity index, white adipose tissue weight (epididymal, subcutaneous and retroperitoneal) and brown adipose tissue weight. Rats fed with the hypercaloric diet showed short-term and long-term memory impairments in the NOR test, as well as increased GFAP expression in astrocytes from all analyzed hypothalamic and hippocampal areas. Conclusion: This astrogliosis suggests that the neuroinflammatory response also occurs in the hippocampus and may be involved in the memory losses observed in obese/overweight animals.

Working Memory in Aphasia: Considering Discourse Processing and Treatment Implications

2017 ◽  
Vol 38 (01) ◽  
pp. 040-051 ◽  
Author(s):  
Amy Henderson ◽  
Hana Kim ◽  
Stephen Kintz ◽  
Nicole Frisco ◽  
Heather Wright
Keyword(s):  
Working Memory ◽  
Discourse Processing ◽  
Phonological Loop ◽  
Long Term Memory ◽  
Limited Capacity ◽  
Term Memory ◽  
Memory Impairments ◽  
Episodic Buffer ◽  
Visuospatial Sketchpad

Evidence suggests that persons with aphasia (PWAs) present with working memory impairments that affect a variety of language tasks. Most of these studies have focused on the phonological loop component of working memory and little attention has been paid to the episodic buffer component. The episodic buffer, as a limited capacity, multimodal system that binds and integrates information from the phonological loop, visuospatial sketchpad, and long-term memory would likely be involved in discourse processing. The purposes of this article were to (1) review discourse level deficits associated with aphasia, (2) describe how a deficit at the level of the episodic buffer could cause such deficits, (3) to review discourse treatment approaches for PWAs, and (4) present preliminary results from a novel discourse treatment study for PWAs.

scholarly journals Deleting HDAC3 rescues long-term memory impairments induced by disruption of the neuron-specific chromatin remodeling subunit BAF53b

2018 ◽  
Vol 25 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Guanhua Shu ◽  
Enikö A. Kramár ◽  
Alberto J. López ◽  
Grace Huynh ◽  
Marcelo A. Wood ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Impairments
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