scholarly journals Preischemic treadmill exercise improves short-term memory by inhibiting hypoperfusion-induced disruption of blood-brain barrier after bilateral common carotid arteries occlusion

2019 ◽  
Vol 15 (3) ◽  
pp. 370-376 ◽  
Author(s):  
Jae-Min Lee ◽  
Seung-Soo Baek ◽  
Tae-Woon Kim ◽  
Hye-Sang Park ◽  
Sang-Seo Park ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Carotid Arteries ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Brain Barrier ◽  
Short Term ◽  
Term Memory ◽  
Blood Brain ◽  
Common Carotid Arteries

Benzophenone-3 Passes Through the Blood-Brain Barrier, Increases the Level of Extracellular Glutamate, and Induces Apoptotic Processes in the Hippocampus and Frontal Cortex of Rats

2019 ◽  
Vol 171 (2) ◽  
pp. 485-500 ◽  
Author(s):  
Bartosz Pomierny ◽  
Weronika Krzyżanowska ◽  
Żaneta Broniowska ◽  
Beata Strach ◽  
Beata Bystrowska ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Blood Brain Barrier ◽  
Brain Structures ◽  
Glutamate Transporters ◽  
Brain Barrier ◽  
Short Term ◽  
Extracellular Glutamate ◽  
Blood Brain ◽  
The Impact ◽  
The Brain

Abstract Benzophenone-3 is the most commonly used UV filter. It is well absorbed through the skin and gastrointestinal tract. Its best-known side effect is the impact on the function of sex hormones. Little is known about the influence of BP-3 on the brain. The aim of this study was to show whether BP-3 crosses the blood-brain barrier (BBB), to determine whether it induces nerve cell damage in susceptible brain structures, and to identify the mechanism of its action in the central nervous system. BP-3 was administered dermally during the prenatal period and adulthood to rats. BP-3 effect on short-term and spatial memory was determined by novel object and novel location recognition tests. BP-3 concentrations were assayed in the brain and peripheral tissues. In brain structures, selected markers of brain damage were measured. The study showed that BP-3 is absorbed through the rat skin, passes through the BBB. BP-3 raised oxidative stress and induced apoptosis in the brain. BP-3 increased the concentration of extracellular glutamate in examined brain structures and changed the expression of glutamate transporters. BP-3 had no effect on short-term memory but impaired spatial memory. The present study showed that dermal BP-3 exposure may cause damage to neurons what might be associated with the increase in the level of extracellular glutamate, most likely evoked by changes in the expression of GLT-1 and xCT glutamate transporters. Thus, exposure to BP-3 may be one of the causes that increase the risk of developing neurodegenerative diseases.

Treadmill exercise improves short-term memory by suppressing ischemia-induced apoptosis of neuronal cells in gerbils

2004 ◽  
Vol 372 (3) ◽  
pp. 256-261 ◽  
Author(s):  
Young-Je Sim ◽  
Sung-Soo Kim ◽  
Jee-Youn Kim ◽  
Mal-Soon Shin ◽  
Chang-Ju Kim
Keyword(s):  
Short Term Memory ◽  
Treadmill Exercise ◽  
Neuronal Cells ◽  
Short Term ◽  
Term Memory ◽  
Induced Apoptosis

scholarly journals Adenosine A2A receptor agonist polydeoxyribonucleotide ameliorates short-term memory impairment by suppressing cerebral ischemia-induced inflammation via MAPK pathway

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248689
Author(s):  
Il-Gyu Ko ◽  
Jun-Jang Jin ◽  
Lakkyong Hwang ◽  
Sang-Hoon Kim ◽  
Chang-Ju Kim ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Inflammatory Cytokines ◽  
Memory Impairment ◽  
Carotid Arteries ◽  
Short Term Memory ◽  
Mapk Signaling ◽  
Short Term ◽  
The Common ◽  
Common Carotid Arteries ◽  
Pro Inflammatory Cytokines

Cerebral ischemia causes tissue death owing to occlusion of the cerebral blood vessels, and cerebral ischemia activates mitogen-activated protein kinase (MAPK) and induces secretion of pro-inflammatory cytokines. Adenosine A2A receptor agonist, polydeoxyribonucleotide (PDRN), suppresses the secretion of pro-inflammatory cytokines and exhibits anti-inflammatory effect. In the current study, the therapeutic effect of PDRN on cerebral ischemia was evaluated using gerbils. For the induction of cerebral ischemia, the common carotid arteries were exposed, and then aneurysm clips were used to occlude the common carotid arteries bilaterally for 7 minutes. In the PDRN-treated groups, the gerbils were injected intraperitoneally with 0.3 mL of saline containing 8 mg/kg PDRN, per a day for 7 days following cerebral ischemia induction. In order to confirm the participation of the adenosine A2A receptor in the effects mediated by PDRN, 8 mg/kg 7-dimethyl-1-propargylxanthine (DMPX), adenosine A2A receptor antagonist, was treated with PDRN. In the current study, induction of ischemia enhanced the levels of pro-inflammatory cytokines and increased phosphorylation of MAPK signaling factors in the hippocampus and basolateral amygdala. However, treatment with PDRN ameliorated short-term memory impairment by suppressing the production of pro-inflammatory cytokines and inactivation of MAPK signaling factors in cerebral ischemia. Furthermore, PDRN treatment enhanced the concentration of cyclic adenosine-3,5’-monophosphate (cAMP) as well as phosphorylation of cAMP response element-binding protein (p-CREB). Co-treatment of DMPX and PDRN attenuated the therapeutic effect of PDRN on cerebral ischemia. Based on these findings, PDRN may be developed as the primary treatment in cerebral ischemia.

scholarly journals Treadmill exercise improves short-term memory by enhancing neurogenesis in amyloid beta-induced Alzheimer disease rats

2014 ◽  
Vol 10 (1) ◽  
pp. 2-8 ◽  
Author(s):  
Bo-Kyun Kim ◽  
Mal-Soon Shin ◽  
Chang-Ju Kim ◽  
Sang-Bin Baek ◽  
Yeong-Chan Ko ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Amyloid Beta ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Short Term ◽  
Term Memory

scholarly journals Effects of treadmill exercise on activity, short-term memory, vascular dysfunction in maternal separation rats

2020 ◽  
Vol 16 (2) ◽  
pp. 118-123 ◽  
Author(s):  
Sang-Seo Park ◽  
Tae-Woon Kim ◽  
Hye-Sang Park ◽  
Tae-Beom Seo ◽  
Young-Pyo Kim
Keyword(s):  
Maternal Separation ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Vascular Dysfunction ◽  
Short Term ◽  
Term Memory

scholarly journals Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

2020 ◽  
Author(s):  
Dina Monir ◽  
Motamed Mahmoud ◽  
Omyma Galal ◽  
Ibrahim Rehan ◽  
Amany Abdelrahman
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Neurodegenerative Disorder ◽  
Short Term ◽  
Term Memory ◽  
Nrf2 Pathway

Abstract Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism.This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of NRF2-ARE pathway as a mechanism involved in exercise associated improvement in rotenone rat model of PD.Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination) groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone model of PD. When treadmill exercise introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor co-ordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to NRF2 pathways such as TFAM, NRF2, Noq.1 mRNA expression.Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating NRF2 pathway.

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