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.

scholarly journals Calcium-Stimulated Adenylyl Cyclase Activity Is Critical for Hippocampus-Dependent Long-Term Memory and Late Phase LTP

Neuron ◽  
1999 ◽  
Vol 23 (4) ◽  
pp. 787-798 ◽  
Author(s):  
Scott T Wong ◽  
Jaime Athos ◽  
Xavier A Figueroa ◽  
Victor V Pineda ◽  
Michele L Schaefer ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Late Phase ◽  
Cyclase Activity ◽  
Long Term Memory ◽  
Adenylyl Cyclase Activity ◽  
Term Memory

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.

scholarly journals Genetic Demonstration of a Role for PKA in the Late Phase of LTP and in Hippocampus-Based Long-Term Memory

Cell ◽  
1997 ◽  
Vol 88 (5) ◽  
pp. 615-626 ◽  
Author(s):  
Ted Abel ◽  
Peter V Nguyen ◽  
Mark Barad ◽  
Thomas A.S Deuel ◽  
Eric R Kandel ◽  
...  
Keyword(s):  
Late Phase ◽  
Long Term Memory ◽  
Term Memory

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.

Long-term memory of body weight and past weight satisfaction: a longitudinal follow-up study

1991 ◽  
Vol 53 (6) ◽  
pp. 1493-1498 ◽  
Author(s):  
V A Casey ◽  
J T Dwyer ◽  
C S Berkey ◽  
K A Coleman ◽  
J Gardner ◽  
...  
Keyword(s):  
Body Weight ◽  
Long Term Memory ◽  
Term Memory ◽  
Follow Up Study ◽  
Weight Satisfaction

scholarly journals LIMK1 Regulates Long-Term Memory and Synaptic Plasticity via the Transcriptional Factor CREB

2015 ◽  
Vol 35 (8) ◽  
pp. 1316-1328 ◽  
Author(s):  
Zarko Todorovski ◽  
Suhail Asrar ◽  
Jackie Liu ◽  
Ner Mu Nar Saw ◽  
Krutika Joshi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Williams Syndrome ◽  
Neurodevelopmental Disorder ◽  
Late Phase ◽  
Long Term Potentiation ◽  
Transcriptional Factor ◽  
Adult Brain ◽  
Long Term Memory ◽  
Term Memory

Deletion of theLIMK1gene is associated with Williams syndrome, a unique neurodevelopmental disorder characterized by severe defects in visuospatial cognition and long-term memory (LTM). However, whether LIMK1 contributes to these deficits remains elusive. Here, we show that LIMK1-knockout (LIMK1−/−) mice are drastically impaired in LTM but not short-term memory (STM). In addition, LIMK1−/−mice are selectively defective in late-phase long-term potentiation (L-LTP), a form of long-lasting synaptic plasticity specifically required for the formation of LTM. Furthermore, we show that LIMK1 interacts and regulates the activity of cyclic AMP response element-binding protein (CREB), an extensively studied transcriptional factor critical for LTM. Importantly, both L-LTP and LTM deficits in LIMK1−/−mice are rescued by increasing the activity of CREB. These results provide strong evidence thatLIMK1deletion is sufficient to lead to an LTM deficit and that this deficit is attributable to CREB hypofunction. Our study has identified a direct gene-phenotype link in mice and provides a potential strategy to restore LTM in patients with Williams syndrome through the enhancement of CREB activity in the adult brain.

Sign in / Sign up

Export Citation Format

Share Document