scholarly journals Aquaporin-4 Deficiency Impairs Synaptic Plasticity and Associative Fear Memory in the Lateral Amygdala: Involvement of Downregulation of Glutamate Transporter-1 Expression

2012 ◽  
Vol 37 (8) ◽  
pp. 1867-1878 ◽  
Author(s):  
Yan-Kun Li ◽  
Fang Wang ◽  
Wei Wang ◽  
Yi Luo ◽  
Peng-Fei Wu ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Glutamate Transporter ◽  
Fear Memory ◽  
Aquaporin 4 ◽  
Lateral Amygdala ◽  
Glutamate Transporter 1

scholarly journals Epigenetic Alterations Are Critical for Fear Memory Consolidation and Synaptic Plasticity in the Lateral Amygdala

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e19958 ◽  
Author(s):  
Melissa S. Monsey ◽  
Kristie T. Ota ◽  
Irene F. Akingbade ◽  
Ellie S. Hong ◽  
Glenn E. Schafe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Epigenetic Alterations ◽  
Lateral Amygdala

scholarly journals The Neuroprotective Effect of the Association of Aquaporin-4/Glutamate Transporter-1 against Alzheimer’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Yu-Long Lan ◽  
Shuang Zou ◽  
Jian-Jiao Chen ◽  
Jie Zhao ◽  
Shao Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Ion Homeostasis ◽  
Water Channel ◽  
Glutamate Transporter ◽  
Aquaporin 4 ◽  
Normal Brain ◽  
Glutamate Transporter 1

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is characterized by memory loss and cognitive dysfunction. Aquaporin-4 (AQP4), which is primarily expressed in astrocytes, is the major water channel expressed in the central nervous system (CNS). This protein plays an important role in water and ion homeostasis in the normal brain and in various brain pathological conditions. Emerging evidence suggests that AQP4 deficiency impairs learning and memory and that this may be related to the expression of glutamate transporter-1 (GLT-1). Moreover, the colocalization of AQP4 and GLT-1 has long been studied in brain tissue; however, far less is known about the potential influence that the AQP4/GLT-1 complex may have on AD. Research on the functional interaction of AQP4 and GLT-1 has been demonstrated to be of great significance in the study of AD. Here, we review the interaction of AQP4 and GLT-1 in astrocytes, which might play a pivotal role in the regulation of distinct cellular responses that involve neuroprotection against AD. The association of AQP4 and GLT-1 could greatly supplement previous research regarding neuroprotection against AD.

scholarly journals Different Dynamics of Aquaporin 4 and Glutamate Transporter-1 Distribution in the Perineuronal and Perivascular Compartments during Ischemic Stroke

2014 ◽  
Vol 24 (5) ◽  
pp. 475-493 ◽  
Author(s):  
Laurentiu Mogoanta ◽  
Marius Ciurea ◽  
Ionica Pirici ◽  
Claudiu Margaritescu ◽  
Cristiana Simionescu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Glutamate Transporter ◽  
Aquaporin 4 ◽  
Glutamate Transporter 1

scholarly journals Effects of Co-exposure to Lead and Manganese on Learning and Memory Deficits

2021 ◽  
Author(s):  
Rui-Li Guan ◽  
Tao Wang ◽  
Xiao-Ru Dong ◽  
Ke-Jun Du ◽  
Juan Li ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Real Life ◽  
Glutamate Transporter ◽  
Synaptic Cleft ◽  
Long Term Potentiation ◽  
Metal Exposure ◽  
Combined Exposure ◽  
Sprague Dawley ◽  
Significant Difference ◽  
Glutamate Transporter 1

Abstract Background: Lead and manganese are common neurotoxins. However, individuals are subject to co-exposures in real life, and it is therefore important to study these metals in combination. Methods: Weaning Sprague-Dawley rats were given ad libitum access to drinking water solutions containing lead (100 ppm), manganese (2.5 mg/mL) or a mixture, and each treatment has its own minocycline (50 mg/Kg.d) supplement group. Results: The results showed a significant difference in spatial memory and the induction levels of hippocampal long-term potentiation (LTP) in all exposure groups when compared with controls. The combined exposure group exhibited the most pronounced effect when compared with each of the single metal exposure groups. Microglia displayed activation at day 3 after exposure alone or in combination, while astrocytes showed activation at day 5, accompanied by decreased expression levels of glutamate/aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), and glutamine synthetase (GS). Furthermore, the levels of the glutamate in the synaptic cleft increased significantly. When microglial activation was inhibited by minocycline, the activation of astrocytes, and the expression of GLAST, GLT-1, and GS were both reversed. In addition, upon minocycline treatment, the hippocampal LTP impairment and the cognitive injury were significantly alleviated in each of the exposure groups. Conclusions: These results suggest that combined exposure to lead and manganese can cause greater effects on cognition and synaptic plasticity when compared to single metal exposure groups. And the reason may involve in microglia abnormal activation leading to an excessive regulation of astrocytes, resulting in glutamate reuptake dysfunction in astrocytes and lead to perturbed cognition and synaptic plasticity.

scholarly journals Unaltered Glutamate Transporter-1 Protein Levels in Aquaporin-4 Knockout Mice

ASN NEURO ◽  
2017 ◽  
Vol 9 (1) ◽  
pp. 175909141668784
Author(s):  
Jacqueline A. Hubbard ◽  
Devin K. Binder
Keyword(s):  
Knockout Mice ◽  
Glutamate Transporter ◽  
Aquaporin 4 ◽  
Protein Levels ◽  
Glutamate Transporter 1

scholarly journals Regulation of astrocyte glutamate transporter-1 (GLT1) and aquaporin-4 (AQP4) expression in a model of epilepsy

2016 ◽  
Vol 283 ◽  
pp. 85-96 ◽  
Author(s):  
Jacqueline A. Hubbard ◽  
Jenny I. Szu ◽  
Jennifer M. Yonan ◽  
Devin K. Binder
Keyword(s):  
Glutamate Transporter ◽  
Aquaporin 4 ◽  
Aqp4 Expression ◽  
Glutamate Transporter 1
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