Deterioration in learning and memory of fear conditioning in response to context in aged SAMP8 mice 1 1Abbreviations: SAM, senescence-accelerated mouse; SAMP, senescence-accelerated mouse prone; SAMR, senescence-accelerated mouse resistant; GABA, gamma-aminobutyric acid; MGRF, magnocelluar reticular formation; RSA, hippocampal rhythmic slow activity; CS, conditioned stimulus.

2001 ◽  
Vol 22 (3) ◽  
pp. 479-484 ◽  
Author(s):  
Akira Ohta ◽  
Ichiro Akiguchi ◽  
Naoyuki Seriu ◽  
Katsunori Ohnishi ◽  
Hideo Yagi ◽  
...  
2008 ◽  
Vol 82 (20) ◽  
pp. 9890-9899 ◽  
Author(s):  
Matthew J. Trifilo ◽  
Manuel Sanchez-Alavez ◽  
Laura Solforosi ◽  
Joie Bernard-Trifilo ◽  
Stefan Kunz ◽  
...  

ABSTRACT After infection with RML murine scrapie agent, transgenic (tg) mice expressing prion protein (PrP) without its glycophosphatidylinositol (GPI) membrane anchor (GPI−/− PrP tg mice) continue to make abundant amounts of the abnormally folded disease-associated PrPres but have a normal life span. In contrast, all age-, sex-, and genetically matched mice with a GPI-anchored PrP become moribund and die due to a chronic progressive neurodegenerative disease by 160 days after RML scrapie agent infection. We report here that infected GPI−/− PrP tg mice, although free from progressive neurodegenerative disease of the cerebellum and extrapyramidal and pyramidal systems, nevertheless suffer defects in learning and memory, long-term potentiation, and neuronal excitability. Such dysfunction increases over time and is associated with an increase in gamma aminobutyric acid (GABA) inhibition but not loss of excitatory glutamate/N-methyl-d-aspartic acid. Enhanced deposition of abnormally folded infectious PrP (PrPsc or PrPres) in the central nervous system (CNS) localizes with GABAA receptors. This occurs with minimal evidence of CNS spongiosis or apoptosis of neurons. The use of monoclonal antibodies reveals an association of PrPres with GABAA receptors. Thus, the clinical defects of learning and memory loss in vivo in GPI−/− PrP tg mice infected with scrapie agent may likely involve the GABAergic pathway.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yuan-Yuan Li ◽  
Nan-Qu Huang ◽  
Fei Feng ◽  
Ying Li ◽  
Xiu-Mei Luo ◽  
...  

Icaritin (ICT) is the main component in the traditional Chinese herb Epimedium, and it has been shown to have anti-Alzheimer’s disease (AD) effects, but its neuroprotective effects and the pharmacological mechanisms are unclear. In the present study, senescence-accelerated mouse prone 8 (SAMP8) mice were randomly divided into a model group and an ICT-treated group. Learning and memory abilities were detected by the Morris water maze assay, and the expression of amyloid beta protein (Aβ) and β-site APP cleavage enzyme 1 (BACE1) was determined by Western blotting and polymerase chain reaction (PCR). Histological changes in CA1 and CA3 were detected by hematoxylin-eosin staining (H&E staining), and the immunohistochemical analysis was used to detect the expression and localization of Bax and Bcl-2. The results showed that compared with the SAMP8 mice, the ICT-treated SAMP8 mice showed improvements in spatial learning and memory retention. In addition, the number of necrotic cells and the morphological changes in CA1 and CA3 areas were significantly alleviated in the group of ICT-treated SAMP8 mice, and the expression of BACE1, Aβ1-42 levels, and the Bax/Bcl-2 ratio in the hippocampus was obviously decreased in the ICT-treated group compared with the control group. The results demonstrated that ICT reduced BACE-1 levels, the contents of Aβ1-42, and the Bax/Bcl-2 ratio, suggesting that ICT might have potential therapeutic benefits by delaying or modifying the progression of AD.


2021 ◽  
Author(s):  
Eri Sumiyoshi ◽  
Michio Hashimoto ◽  
Shahdat Hossain ◽  
Kentaro Matsuzaki ◽  
Rafiad Islam ◽  
...  

Anredera cordifolia extract increased learning and memory by enhancing levels of hippocampal BDNF, PSD95, NR2A, and p-CREB in SAMP8 mice.


Author(s):  
Kazunori Sasaki ◽  
Noelia Geribaldi-Doldán ◽  
Qingqing Wu ◽  
Julie Davies ◽  
Francis G. Szele ◽  
...  

Much attention has recently been focused on nutraceuticals, with minimal adverse effects, developed for preventing or treating neurological diseases such as Alzheimer's disease (AD). The present study was conducted to investigate the potential effect on neural development and function of the microalgae Aurantiochytrium sp. as a nutraceutical. To test neuroprotection by the ethanol extract of Aurantiochytrium (EEA) and a derivative, the n-Hexane layer of EEA (HEEA), amyloid-β-stimulated SH-SY5Y cells, was used as an in vitro AD model. We then assessed the potential enhancement of neurogenesis by EEA and HEEA using murine ex vivo neurospheres. We also administered EEA or HEEA to senescence-accelerated mouse-prone 8 (SAMP8) mice, a non-transgenic strain with accelerated aging and AD-like memory loss for evaluation of spatial learning and memory using the Morris water maze test. Finally, we performed immunohistochemical analysis for assessment of neurogenesis in mice administered EEA. Pretreatment of SH-SY5Y cells with EEA or the squalene-rich fraction of EEA, HEEA, ameliorated amyloid-β-induced cytotoxicity. Interestingly, only EEA-treated cells showed a significant increase in cell metabolism and intracellular adenosine triphosphate production. Moreover, EEA treatment significantly increased the number of neurospheres, whereas HEEA treatment significantly increased the number of β-III-tubulin+ young neurons and GFAP+ astrocytes. SAMP8 mice were given 50 mg/kg EEA or HEEA orally for 30 days. EEA and HEEA decreased escape latency in the Morris water maze in SAMP8 mice, indicating improved memory. To detect stem cells and newborn neurons, we administered BrdU for 9 days and measured BrdU+ cells in the dentate gyrus, a neurogenic stem cell niche of the hippocampus. In SAMP8 mice, EEA rapidly and significantly increased the number of BrdU+GFAP+ stem cells and their progeny, BrdU+NeuN+ mature neurons. In conclusion, our data in aggregate indicate that EEA and its constituents could be developed into a nutraceutical for promoting brain health and function against several age-related diseases, particularly AD.


Author(s):  
Laxminarayana Kurady Bairy ◽  
Suresh Kumar

Learning and memory being highly specialized process of human brain involves complex interaction between neurotransmitters and cellular events. Over the years, the understandings of these processes have been evolving from psychological, neurophysiological, and pharmacological perspectives. The most widely appraised model of learning and memory involves attention, acquisition, storage and retrieval. Each of these events involve interplay of neurotransmitters such as dopamine, acetylcholine, norepinephrine, N-methyl-d-aspartic acid, gamma-aminobutyric acid, though preponderance of specific neurotransmitter have been documented. The formation of long-term memory involves cellular events with neuroplasticity. Further, dopamine is documented to play crucial role in the process of forgetting. Understanding of the processes of learning and memory not only facilitates drug discovery, but also helps to understand actions of several existing drugs. In addition, it would also help to enhance psychological interventions in children with learning disabilities. Thus, the review intends to summarize role of neurotransmitters and neuromodulators during different phases of learning and memory.


Sign in / Sign up

Export Citation Format

Share Document