scholarly journals Dietary Starch Composition Effects on Cx43-intercellular Communication Channels and Short-Term Memory

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1205-1205
Author(s):  
Sarah Francisco ◽  
Kelsey Smith ◽  
Sheldon Rowan ◽  
Gemma Aragonès Bargalló ◽  
Donald Smith ◽  
...  

Abstract Objectives Intercellular communication mediated by gap junctions is critical for cognitive and sensory functions and is disturbed with age and age-related diseases. We analyzed the impact of consuming a high glycemic diet or a low glycemic dietary intervention on Cx43, a component of gap junction intercellular communication channels associated with spatial short-term memory, in different age groups of mice. Methods Male C57Bl6/J mice (n = 12–13) aged 7 months were fed equal amounts of either a high glycemic (HG) diet or a low glycemic (LG) diet for 1 month or 9 months. Within the 9-month feeding trial, half of the HG-fed animals were switched to the LG diet (HGxLG) at 4.5 months. The diets are isocaloric, but the HG starch is 100% composed of amylopectin, and the LG diet contains a 30% amylopectin/70% amylose mixture of starch and is digested much slower. We also analyzed tissues from a previous feeding trial where 12-month aged animals were fed these same diets over 12 months. The animals were weighed weekly, underwent intraperitoneal glucose tolerance tests to evaluate glycemic response, were tested for cognition using a novel object recognition test, and tissues were collected. Tissues including brain and eye samples were evaluated for Cx43, a component of gap junction intercellular communication channels, using immunohistochemistry and western blotting. Results At both time points, compared to the LG-fed controls, the HG-fed animals had significantly increased (>10%) body weight, while the HGxLG crossover animals’ body weight did not differ significantly from the LG-fed controls at 15 months. At 14 months, there was no significant difference in novel object recognition, although there was a trend of improved novel object recognition in the HGxLG crossover group. Cx43 gap junction protein accumulated in eye tissues of the HG-fed animals, and this accumulation was attenuated in the HGxLG group. Conclusions These results suggest that detrimental consequences of a high glycemic diet during aging on cognitive function may be reversible, supporting that a switch in dietary habits may be an effective nutritional intervention in older adults. Funding Sources USDA JM HNRCA Pilot Grant Program, NIH, USDA NIFA, USDA, Thome Memorial Foundation, and the BrightFocus Foundation.

2020 ◽  
Vol 178 (2) ◽  
pp. 347-357
Author(s):  
Muhammad M Hossain ◽  
Abdelmadjid Belkadi ◽  
Sara Al-Haddad ◽  
Jason R Richardson

Abstract Deficits in learning and memory are often associated with disruption of hippocampal neurogenesis, which is regulated by numerous processes, including precursor cell proliferation, survival, migration, and differentiation to mature neurons. Recent studies demonstrate that adult born neurons in the dentate gyrus (DG) in the hippocampus can functionally integrate into the existing neuronal circuitry and contribute to hippocampal-dependent learning and memory. Here, we demonstrate that relatively short-term deltamethrin exposure (3 mg/kg every 3 days for 1 month) inhibits adult hippocampal neurogenesis and causes deficits in learning and memory in mice. Hippocampal-dependent cognitive functions were evaluated using 2 independent hippocampal-dependent behavioral tests, the novel object recognition task and Morris water maze. We found that deltamethrin-treated mice exhibited profound deficits in novel object recognition and learning and memory in water maze. Deltamethrin exposure significantly decreased bromodeoxyuridine (BrdU)-positive cells (39%) and Ki67+ cells (47%) in the DG of the hippocampus, indicating decreased cellular proliferation. In addition, deltamethrin-treated mice exhibited a 44% decrease in nestin-expressing neural progenitor cells and a 38% reduction in the expression of doublecortin (DCX), an early neuronal differentiation marker. Furthermore, deltamethrin-exposed mice exhibited a 25% reduction in total number of granule cells in the DG. These findings indicate that relatively short-term exposure to deltamethrin causes significant deficits in hippocampal neurogenesis that is associated with impaired learning and memory.


2013 ◽  
Vol 105 ◽  
pp. 174-185 ◽  
Author(s):  
Shannon J. Moore ◽  
Kaivalya Deshpande ◽  
Gwen S. Stinnett ◽  
Audrey F. Seasholtz ◽  
Geoffrey G. Murphy

2021 ◽  
Vol 13 ◽  
Author(s):  
Angelina Lesnikova ◽  
Plinio Casarotto ◽  
Rafael Moliner ◽  
Senem Merve Fred ◽  
Caroline Biojone ◽  
...  

Perineuronal nets (PNNs) have an important physiological role in the retention of learning by restricting cognitive flexibility. Their deposition peaks after developmental periods of intensive learning, usually in late childhood, and they help in long-term preservation of newly acquired skills and information. Modulation of PNN function by various techniques enhances plasticity and regulates the retention of memories, which may be beneficial when memory persistence entails negative symptoms such as post-traumatic stress disorder (PTSD). In this study, we investigated the role of PTPσ [receptor-type tyrosine-protein phosphatase S, a phosphatase that is activated by binding of chondroitin sulfate proteoglycans (CSPGs) from PNNs] in retention of memories using Novel Object Recognition and Fear Conditioning models. We observed that mice haploinsufficient for PTPRS gene (PTPσ+/–), although having improved short-term object recognition memory, display impaired long-term memory in both Novel Object Recognition and Fear Conditioning paradigm, as compared to WT littermates. However, PTPσ+/– mice did not show any differences in behavioral tests that do not heavily rely on cognitive flexibility, such as Elevated Plus Maze, Open Field, Marble Burying, and Forced Swimming Test. Since PTPσ has been shown to interact with and dephosphorylate TRKB, we investigated activation of this receptor and its downstream pathways in limbic areas known to be associated with memory. We found that phosphorylation of TRKB and PLCγ are increased in the hippocampus, prefrontal cortex, and amygdaloid complex of PTPσ+/– mice, but other TRKB-mediated signaling pathways are not affected. Our data suggest that PTPσ downregulation promotes TRKB phosphorylation in different brain areas, improves short-term memory performance but disrupts long-term memory retention in the tested animal models. Inhibition of PTPσ or disruption of PNN-PTPσ-TRKB complex might be a potential target for disorders where negative modulation of the acquired memories can be beneficial.


2021 ◽  
Vol 12 (1) ◽  
pp. 22-28
Author(s):  
Saeed Mustapha ◽  
◽  
Majidat Oshafu ◽  
Umar Adam ◽  
Yusuf Yusha’u ◽  
...  

Depression is among the most prevalent diseases worldwide. Researchers have identified a link between depression and different types of memory loss, including short term memory (STM). Also, the memory impairment in depression is a function of severity. This study was conducted to evaluate the effect of antidepressant medication on short term memory in chronic mild stress (CMS) mouse model of depression. A total of eighteen female mice were randomly divided into three groups of six mice each (n=6). Group I served as normal control, group II were exposed to CMS for 14 days, group III were exposed to CMS for 14 days, and thereafter treated with paroxetine at a dose of 20 mg/kg for 14 days. Short term memory was assessed using batteries of cognitive tests including the Y-maze and novel object recognition. Further antidepressant effect was measured using the tail suspension test (TST). The results showed that paroxetine at 20 mg/kg significantly improved the short term memory of the depressed female mice (p<0.05) in the Y-maze and novel object (recognition) tasks after CMS. Therefore, paroxetine might be used to enhance short term memory in depressed individuals, although clinical studies are required to confirm this finding.


2021 ◽  
Author(s):  
Ivonne Becker ◽  
Lihua Wang‐Eckhardt ◽  
Julia Lodder‐Gadaczek ◽  
Yong Wang ◽  
Agathe Grünewald ◽  
...  

2001 ◽  
Vol 280 (2) ◽  
pp. L191-L202 ◽  
Author(s):  
Yihe Guo ◽  
Cara Martinez-Williams ◽  
Clare E. Yellowley ◽  
Henry J. Donahue ◽  
D. Eugene Rannels

Extracellular matrix (ECM) proteins promote attachment, spreading, and differentiation of cultured alveolar type II epithelial cells. The present studies address the hypothesis that the ECM also regulates expression and function of gap junction proteins, connexins, in this cell population. Expression of cellular fibronectin and connexin (Cx) 43 increase in parallel during early type II cell culture as Cx26 expression declines. Gap junction intercellular communication is established over the same interval. Cells plated on a preformed, type II cell-derived, fibronectin-rich ECM demonstrate accelerated formation of gap junction plaques and elevated gap junction intercellular communication. These effects are blocked by antibodies against fibronectin, which cause redistribution of Cx43 protein from the plasma membrane to the cytoplasm. Conversely, cells cultured on a laminin-rich ECM, Matrigel, express low levels of Cx43 but high levels of Cx26, reflecting both transcriptional and translational regulation. Cx26 and Cx43 thus demonstrate reciprocal regulation by ECM constituents.


2015 ◽  
Vol 34 (4) ◽  
pp. 2133-2141 ◽  
Author(s):  
LINGZHI WANG ◽  
JIANXIN PENG ◽  
HUANSEN HUANG ◽  
QIN WANG ◽  
MEILING YU ◽  
...  

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