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 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.

miR-124 upregulates astrocytic glutamate transporter-1 via the Akt and mTOR signaling pathway post ischemic stroke

2019 ◽  
Vol 149 ◽  
pp. 231-239 ◽  
Author(s):  
Wei-Yi Huang ◽  
Chen Jiang ◽  
Han-Bin Ye ◽  
Jian-Tong Jiao ◽  
Chao Cheng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Glutamate Transporter ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Glutamate Transporter 1

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

scholarly journals Ischemia-Induced Cognitive Impairment Is Improved via Remyelination and Restoration of Synaptic Density in the Hippocampus after Treatment with COG-Up® in a Gerbil Model of Ischemic Stroke

2021 ◽  
Vol 8 (12) ◽  
pp. 321
Author(s):  
Tae-Kyeong Lee ◽  
Junkee Hong ◽  
Ji-Won Lee ◽  
Sung-Su Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter ◽  
Synaptic Density ◽  
Ca1 Region ◽  
Fluoro Jade B ◽  
Glutamate Transporter 1

Cerebrovascular disease such as ischemic stroke develops cognitive impairment due to brain tissue damage including neural loss, demyelination and decrease in synaptic density. In the present study, we developed transient ischemia in the forebrain of the gerbil and found cognitive impairment using the Barnes maze test and passive avoidance test for spatial memory and learning memory, respectively. In addition, neuronal loss/death was detected in the Cornu Ammonis 1 (CA1) region of the gerbil hippocampus after the ischemia by cresyl violet histochemistry, immunohistochemistry for neuronal nuclei and histofluorescence with Fluoro-Jade B. Furthermore, in the CA1 region following ischemia, myelin and vesicular synaptic density were significantly decreased using immunohistochemistry for myelin basic protein and vesicular glutamate transporter 1. In the gerbils, treatment with COG-up® (a combined extract of Erigeron annuus (L.) Pers. and Brassica oleracea Var.), which was rich in scutellarin and sinapic acid, after the ischemia, significantly improved ischemia-induced decline in memory function when compared with that shown in gerbils treated with vehicle after the ischemia. In the CA1 region of these gerbils, COG-up® treatment significantly promoted the remyelination visualized using immunohistochemistry myelin basic protein, increased oligodendrocytes visualized using a receptor-interacting protein, and restored the density of glutamatergic synapses visualized using double immunofluorescence for vesicular glutamate transporter 1 and microtubule-associated protein, although COG-up® treatment did not protect pyramidal cells (principal neurons) located in the CA1 region form the ischemic insult. Considering the current findings, a gerbil model of ischemic stroke apparently showed cognitive impairment accompanied by ischemic injury in the hippocampus; also, COG-up® can be employed for improving cognitive decline following ischemia-reperfusion injury in brains.

Cerebrolysin and Aquaporin 4 Inhibition Improve Pathological and Motor Recovery after Ischemic Stroke

2018 ◽  
Vol 17 (4) ◽  
pp. 299-308 ◽  
Author(s):  
Bogdan Catalin ◽  
Otilia-Constantina Rogoveanu ◽  
Ionica Pirici ◽  
Tudor Adrian Balseanu ◽  
Adina Stan ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Vasogenic Edema ◽  
Artery Occlusion ◽  
Aquaporin 4 ◽  
Hypertonic Solution ◽  
Water Metabolism ◽  
Scar Region ◽  
Function Preservation ◽  
Neurotropic Factor ◽  
Cerebral Artery Occlusion

Background: Edema represents one of the earliest negative markers of survival and consecutive neurological deficit following stroke. The mixture of cellular and vasogenic edema makes treating this condition complicated, and to date, there is no pathogenically oriented drug treatment for edema, which leaves parenteral administration of a hypertonic solution as the only non-surgical alternative. Objective: New insights into water metabolism in the brain have opened the way for molecular targeted treatment, with aquaporin 4 channels (AQP4) taking center stage. We aimed here to assess the effect of inhibiting AQP4 together with the administration of a neurotropic factor (Cerebrolysin) in ischemic stroke. Methods: Using a permanent medial cerebral artery occlusion rat model, we administrated a single dose of the AQP4 inhibitor TGN-020 (100 mg/kg) at 15 minutes after ischemia followed by daily Cerebrolysin dosing (5ml/kg) for seven days. Rotarod motor testing and neuropathology examinations were next performed. Results: We showed first that the combination treatment animals have a better motor function preservation at seven days after permanent ischemia. We have also identified distinct cellular contributions that represent the bases of behavior testing, such as less astrocyte scarring and a larger neuronalsurvival phenotype rate in animals treated with both compounds than in animals treated with Cerebrolysin alone or untreated animals. Conclusion: Our data show that water diffusion inhibition and Cerebrolysin administration after focal ischemic stroke reduces infarct size, leading to a higher neuronal survival in the peri-core glial scar region.

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