scholarly journals Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Victor Manuel Blanco-Alvarez ◽  
Guadalupe Soto-Rodriguez ◽  
Juan Antonio Gonzalez-Barrios ◽  
Daniel Martinez-Fong ◽  
Eduardo Brambila ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Growth Factors ◽  
Neural Plasticity ◽  
Memory Loss ◽  
Male Rats ◽  
Long Term Memory ◽  
Cerebral Hypoxia ◽  
Term Memory ◽  
Hypoxia Ischemia

Prophylactic subacute administration of zinc decreases lipoperoxidation and cell death following a transient cerebral hypoxia-ischemia, thus suggesting neuroprotective and preconditioning effects. Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia. We explored whether zinc prevents the cerebral cortex-hippocampus injury through regulation of CCL2, CCR2, FGF2, and IGF-1 expression following a 10 min of common carotid artery occlusion (CCAO). Male rats were grouped as follows: (1) Zn96h, rats injected with ZnCl2(one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnCl2before CCAO; (3) CCAO, rats with CCAO only; (4) Sham group, rats with mock CCAO; and (5) untreated rats. The cerebral cortex-hippocampus was dissected at different times before and after CCAO. CCL2/CCR2, FGF2, and IGF-1 expression was assessed by RT-PCR and ELISA. Learning in Morris Water Maze was achieved by daily training during 5 days. Long-term memory was evaluated on day 7 after learning. Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat. These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

scholarly journals Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Constantino Tomas-Sanchez ◽  
Victor Manuel Blanco-Alvarez ◽  
Juan Antonio Gonzalez-Barrios ◽  
Daniel Martinez-Fong ◽  
Guadalupe Garcia-Robles ◽  
...  
Keyword(s):  
Nitrosative Stress ◽  
Chronic Administration ◽  
Fold Increase ◽  
Atomic Absorption Spectrophotometry ◽  
Artery Occlusion ◽  
Long Term Memory ◽  
Neuroprotective Effects ◽  
Term Memory ◽  
Hypoxia Ischemia

Acute and subacute administration of zinc exert neuroprotective effects in hypoxia-ischemia animal models; yet the effect of chronic administration of zinc still remains unknown. We addressed this issue by injecting zinc at a tolerable dose (0.5 mg/kg weight, i.p.) for 14 days before common carotid artery occlusion (CCAO) in a rat. After CCAO, the level of zinc was measured by atomic absorption spectrophotometry, nitrites were determined by Griess method, lipoperoxidation was measured by Gerard-Monnier assay, and mRNA expression of 84 genes coding for cytokines, chemokines, and their receptors was measured by qRT-PCR, whereas nitrotyrosine, chemokines, and their receptors were assessed by ELISA and histopathological changes in the temporoparietal cortex-hippocampus at different time points. Long-term memory was evaluated using Morris water maze. Following CCAO, a significant increase in nitrosative stress, inflammatory chemokines/receptors, and cell death was observed after 8 h, and a 2.5-fold increase in zinc levels was detected after 7 days. Although CXCL12 and FGF2 protein levels were significantly increased, the long-term memory was impaired 12 days after reperfusion in the Zn+CCAO group. Our data suggest that the chronic administration of zinc at tolerable doses causes nitrosative stress, toxic zinc accumulation, and neuroinflammation, which might account for the neuronal death and cerebral dysfunction after CCAO.

Developmental exposure to methylmercury elicits early cell death in the cerebral cortex and long‐term memory deficits in the rat

2008 ◽  
Vol 27 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Luca Ferraro ◽  
Maria Cristina Tomasini ◽  
Sergio Tanganelli ◽  
Roberta Mazza ◽  
Addolorata Coluccia ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Cortex ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Developmental Exposure ◽  
Term Memory

Facing a Long-Term Memory Loss

2011 ◽  
Vol 39 (2) ◽  
pp. 53-54
Author(s):  
Kevin Mccarty
Keyword(s):  
Memory Loss ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Methamphetamine Inhibits Long-Term Memory Acquisition and Synaptic Plasticity by Evoking Endoplasmic Reticulum Stress

2021 ◽  
Vol 14 ◽  
Author(s):  
Guang Chen ◽  
Xiaoning Wei ◽  
Xiang Xu ◽  
Gang Yu ◽  
Zheng Yong ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Er Stress ◽  
Memory Loss ◽  
Translation Initiation Factor ◽  
Long Term Memory ◽  
Term Memory ◽  
Expression Levels ◽  
Memory Acquisition

Methamphetamine (MA), an illicit drug abused worldwide, leads to cognitive impairment and memory loss. However, the detailed mechanisms of MA-induced neurologic impairment are still unclear. The present study aimed to investigate the mechanisms of MA-induced inhibition of memory acquisition from the perspective of endoplasmic reticulum (ER) stress. ER stress, caused by the accumulation of wrongly folded proteins in the ER, is important for new protein synthesis, which further influence the formation of long-term memory. A subacute MA poisoning model of mice was established and several behavioral experiments were performed, including elevated plus maze, Morris water maze, electro-stimulus Y-maze, and novel object recognition tasks. The present results suggested that 4 days exposure to MA induced significant memory loss. Whereas, this damage to memory formation could be protected when mice were pre-treated with ER stress inhibitor, tauroursodeoxycholic acid (TUDCA). The results of Western blotting showed that subacute exposure to MA increased the expression levels of ER stress marker proteins, such as binding immunoglobulin protein, phosphorylated eukaryotic translation initiation factor 2α, cyclic AMP-dependent transcription factor (ATF)-4, ATF-6, and CCAAT-enhancer binding protein homologous protein. Meanwhile, the enhanced expression levels of these proteins were reversed by TUDCA, indicating that MA administration induced memory loss by evoking ER stress in the hippocampus. We also found that MA inhibited the induction of long-term potentiation (LTP) in the hippocampus. Nevertheless, LTP could be induced when mice were pre-treated with TUDCA. In conclusion, MA inhibited long-term memory acquisition and synaptic plasticity via ER stress.

scholarly journals Early Long-Term Memory Impairment and Changes in the Expression of Synaptic Plasticity-Associated Genes, in the McGill-R-Thy1-APP Rat Model of Alzheimer's-Like Brain Amyloidosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Martín Habif ◽  
Sonia Do Carmo ◽  
María Verónica Báez ◽  
Natalia Claudia Colettis ◽  
Magalí Cecilia Cercato ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Memory Deficits ◽  
Male Rats ◽  
Long Term Memory ◽  
Aβ Oligomers ◽  
Term Memory ◽  
Early Stages ◽  
Human Pathology

Accruing evidence supports the hypothesis that memory deficits in early Alzheimer Disease (AD) might be due to synaptic failure caused by accumulation of intracellular amyloid beta (Aβ) oligomers, then secreted to the extracellular media. Transgenic mouse AD models provide valuable information on AD pathology. However, the failure to translate these findings to humans calls for models that better recapitulate the human pathology. McGill-R-Thy1-APP transgenic (Tg) rat expresses the human amyloid precursor protein (APP751) with the Swedish and Indiana mutations (of familial AD), leading to an AD-like slow-progressing brain amyloid pathology. Therefore, it offers a unique opportunity to investigate learning and memory abilities at early stages of AD, when Aβ accumulation is restricted to the intracellular compartment, prior to plaque deposition. Our goal was to further investigate early deficits in memory, particularly long-term memory in McGill-R-Thy1-APP heterozygous (Tg+/–) rats. Short-term- and long-term habituation to an open field were preserved in 3-, 4-, and 6-month-old (Tg+/–). However, long-term memory of inhibitory avoidance to a foot-shock, novel object-recognition and social approaching behavior were seriously impaired in 4-month-old (Tg+/–) male rats, suggesting that they are unable to either consolidate and/or evoke such associative and discriminative memories with aversive, emotional and spatial components. The long-term memory deficits were accompanied by increased transcript levels of genes relevant to synaptic plasticity, learning and memory processing in the hippocampus, such as Grin2b, Dlg4, Camk2b, and Syn1. Our findings indicate that in addition to the previously well-documented deficits in learning and memory, McGill-R-Thy1-APP rats display particular long-term-memory deficits and deep social behavior alterations at pre-plaque early stages of the pathology. This highlights the importance of Aβ oligomers and emphasizes the validity of the model to study AD-like early processes, with potentially predictive value.

scholarly journals Prophylactic Zinc and Therapeutic Selenium Administration Increases the Antioxidant Enzyme Activity in the Rat Temporoparietal Cortex and Improves Memory after a Transient Hypoxia-Ischemia

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Constantino Tomas-Sanchez ◽  
Victor-Manuel Blanco-Alvarez ◽  
Daniel Martinez-Fong ◽  
Juan-Antonio Gonzalez-Barrios ◽  
Alejandro Gonzalez-Vazquez ◽  
...  
Keyword(s):  
Body Weight ◽  
Late Phase ◽  
Neuronal Cell ◽  
Morris Water Maze Test ◽  
Long Term Memory ◽  
Term Memory ◽  
Prophylactic Administration ◽  
Hypoxia Ischemia ◽  
Therapeutic Administration

In the cerebral hypoxia-ischemia rat model, the prophylactic administration of zinc can cause either cytotoxicity or preconditioning effect, whereas the therapeutic administration of selenium decreases the ischemic damage. Herein, we aimed to explore whether supplementation of low doses of prophylactic zinc and therapeutic selenium could protect from a transient hypoxic-ischemic event. We administrated zinc (0.2 mg/kg of body weight; ip) daily for 14 days before a 10 min common carotid artery occlusion (CCAO). After CCAO, we administrated sodium selenite (6 μg/kg of body weight; ip) daily for 7 days. In the temporoparietal cerebral cortex, we determined nitrites by the Griess method and lipid peroxidation by the Gerard-Monnier assay. qPCR was used to measure mRNA of nitric oxide synthases, antioxidant enzymes, chemokines, and their receptors. We measured the enzymatic activity of SOD and GPx and protein levels of chemokines and their receptors by ELISA. We evaluated long-term memory using the Morris-Water maze test. Our results showed that prophylactic administration of zinc caused a preconditioning effect, decreasing nitrosative/oxidative stress and increasing GPx and SOD expression and activity, as well as eNOS expression. The therapeutic administration of selenium maintained this preconditioning effect up to the late phase of hypoxia-ischemia. Ccl2, Ccr2, Cxcl12, and Cxcr4 were upregulated, and long-term memory was improved. Pyknotic cells were decreased suggesting prevention of neuronal cell death. Our results show that the prophylactic zinc and therapeutic selenium administration induces effective neuroprotection in the early and late phases after CCAO.

Maternal Food Memories in Lin Cheng-sheng's 27°C: Loaf Rock and Eric Khoo's Recipe: A Film on Dementia

2018 ◽  
Vol 18 (4) ◽  
pp. 26-40 ◽  
Author(s):  
Michelle E. Bloom
Keyword(s):  
Cultural Memory ◽  
Short Term Memory ◽  
Chinese Language ◽  
Memory Loss ◽  
Long Term Memory ◽  
Culinary Arts ◽  
Short Term ◽  
Term Memory ◽  
Individual Memory

Elderly mothers pick pineapple in Taiwanese fields and cook curry rice in a Singaporean hawker stand in Lin Cheng-sheng's biopic, 27°C: Loaf Rock, and Eric Khoo's telefilm, Recipe: A Film on Dementia, respectively. Both 2013 Chinese language films employ flashbacks to portray maternal food memories. Lin and Khoo depict food as comforting and possessing a unique ability to stimulate long-term memory to counter the short-term memory loss symptomatic of this form of dementia. The gustatory and the olfactory act directly upon the limbic brain, which houses emotions. In depicting Alzheimer's sufferers and their responses to food, 27°C and Recipe fight for causes. Lin calls attention to the marginalized in his portrayal of the mother succumbing to the disease from the perspective of her son—a character based on contemporary Taiwanese baker Wu Pao-chun, who overcame the adversity of impoverishment to win the world famous Master's de la Boulangerie and found prestigious eponymous bakeries. Parallel to its role in individual memory, food preserves cultural memory. Analogous to culinary arts, cinema, which is made for consumption, combines art and science, embodies culture, and incorporates tradition and innovation, as I show in this comparative study.

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