High-affinity glutamate transporters in the rat retina: a major role of the glial glutamate transporter GLAST-1 in transmitter clearance

1997 ◽  
Vol 291 (1) ◽  
pp. 19-31 ◽  
Author(s):  
T. Rauen ◽  
W. Rowland Taylor ◽  
Kirsten Kuhlbrodt ◽  
Michael Wiessner
2020 ◽  
Author(s):  
Milica Ninkovic ◽  
Mirjana Djukic ◽  
Bojana Mancic ◽  
Petar Milosavljevic ◽  
Ivana Stojanovic ◽  
...  

Abstract Background: Synaptic overload with glutamate aggravates neurotransmission and worsen the progression of the neurodegenerative disease, such as multiple sclerosis (MS). The experimentally induced autoimmune encephalomyelitis (EAE) in rats is a well-established animal model to study MS. Glutamate reuptake occurs by glial glutamate transporter (GLT-1), and glutamate-aspartate transporter (GLAST) localized predominantly in astrocytes terminals. The focus of the study addressing the expression of these transporters in EAE rats and those subjected to theta burst stimulation (TBS), that promotes long-lasting modulation of neuronal activity in rats/humans. Leading by the reported outcomes of TBS, we examined if TBS underlying mechanisms refer to astroglial glutamate transporters status.Methods : We studied changes in the expression of glial glutamate transporter GLT-1 and glutamate-aspartate transporter (GLAST), and glial fibrillary acidic protein (GFAP), in the spinal cord of EAE rats, subjected to intermittent (iTBS) and continuous (cTBS) theta burst stimulation. We quantified the expression of GLAST, GLT-1, and GFAP by immunofluorescence in control and experimental groups of Dark Agouti rats.Results: EAE elevated expression of GFAP, GLAST, and GLT-1. Both TBSs reduced the expression of GFAP. Continual TBS did not interfere with glutamate transporters in EAE rats, while iTBS decreased GLT-1, and increased GLAST.Conclusion: Continual TBS reduced astrogliosis more efficiently than iTBS, in EAE rats. Besides, it did not mitigate the glutamate transporters' expression; thus, glutamate reuptake remained upraised in cTBS exposed EAE rats. Accordingly, we concluded that cTBS might advance the remyelination of damaged neuronal cells in EAE rats. The future clinical trials on the treatment of MS may consider the data of this pre-clinical animal study.


2021 ◽  
Author(s):  
Negin Saeedi ◽  
Mahgol Darvishmolla ◽  
Zohreh Tavassoli ◽  
Shima Davoudi ◽  
Soomaayeh Heysieattalab ◽  
...  

2001 ◽  
Vol 21 (4) ◽  
pp. 404-412 ◽  
Author(s):  
Nathalie Cholet ◽  
Luc Pellerin ◽  
Egbert Welker ◽  
Pierre Lacombe ◽  
Jacques Seylaz ◽  
...  

The mechanisms responsible for the local increase in brain glucose utilization during functional activation remain unknown. Recent in vitro studies have identified a new signaling pathway involving an activation of glial glutamate transporters and enhancement of neuron–astrocyte metabolic interactions that suggest a putative coupling mechanism. The aim of the present study was to determine whether one of the glutamate transporters exclusively expressed in astrocytes, GLAST, is involved in the neurometabolic coupling in vivo. For this purpose, rats were microinjected into the posteromedial barrel subfield (PMBSF) of the somatosensory cortex with GLAST antisense or random phosphorothioate oligonucleotides. The physiologic activation was performed by stimulating the whisker-to-barrel pathway in anesthetized rats while measuring local cerebral glucose utilization by quantitative autoradiography in the PMBSF. Twenty-four hours after injection of two different antisense GLAST oligonucleotide sequences, and despite the presence of normal whisker-related neuronal activity in the PMBSF, the metabolic response to whisker stimulation was decreased by more than 50%. Injection of the corresponding random sequences still allowed a significant increase in glucose utilization in the activated area. The present study highlights the contribution of astrocytes to neurometabolic coupling in vivo. It provides evidence that glial glutamate transporters are key molecular components of this coupling and that neuronal glutamatergic activity is an important determinant of energy utilization. Results indicate that astrocytes should also be considered as possible sources of altered brain metabolism that could explain the distinct imaging signals observed in some pathologic situations


2003 ◽  
Vol 84 (3) ◽  
pp. 522-532 ◽  
Author(s):  
Sachin K. Suchak ◽  
Nicoletta V. Baloyianni ◽  
Michael S. Perkinton ◽  
Robert J. Williams ◽  
Brian S. Meldrum ◽  
...  

2001 ◽  
Vol 78 (2) ◽  
pp. 413-416 ◽  
Author(s):  
Christopher M. Lauderback ◽  
Janna M. Hackett ◽  
Feng F. Huang ◽  
Jeffrey N. Keller ◽  
Luke I. Szweda ◽  
...  

2001 ◽  
Vol 13 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Aclan Dogan ◽  
Kellie K. Bowen ◽  
Kathryn G. Todd ◽  
Robert J. Dempsey

2020 ◽  
Vol 65 (1) ◽  
pp. 28-41
Author(s):  
Marwa Aly Ahmed ◽  
Júlia Erdőssy ◽  
Viola Horváth

Multifunctional nanoparticles have been shown earlier to bind certain proteins with high affinity and the binding affinity could be enhanced by molecular imprinting of the target protein. In this work different initiator systems were used and compared during the synthesis of poly (N-isopropylacrylamide-co-acrylic acid-co-N-tert-butylacrylamide) nanoparticles with respect to their future applicability in molecular imprinting of lysozyme. The decomposition of ammonium persulfate initiator was initiated either thermally at 60 °C or by using redox activators, namely tetramethylethylenediamine or sodium bisulfite at low temperatures. Morphology differences in the resulting nanoparticles have been revealed using scanning electron microscopy and dynamic light scattering. During polymerization the conversion of each monomer was followed in time. Striking differences were demonstrated in the incorporation rate of acrylic acid between the tetramethylethylenediamine catalyzed initiation and the other systems. This led to a completely different nanoparticle microstructure the consequence of which was the distinctly lower lysozyme binding affinity. On the contrary, the use of sodium bisulfite activation resulted in similar nanoparticle structural homogeneity and protein binding affinity as the thermal initiation.


Author(s):  
Stefan Gründer

Acid-sensing ion channels (ASICs) are proton-gated Na+ channels. Being almost ubiquitously present in neurons of the vertebrate nervous system, their precise function remained obscure for a long time. Various animal toxins that bind to ASICs with high affinity and specificity have been tremendously helpful in uncovering the role of ASICs. We now know that they contribute to synaptic transmission at excitatory synapses as well as to sensing metabolic acidosis and nociception. Moreover, detailed characterization of mouse models uncovered an unanticipated role of ASICs in disorders of the nervous system like stroke, multiple sclerosis, and pathological pain. This review provides an overview on the expression, structure, and pharmacology of ASICs plus a summary of what is known and what is still unknown about their physiological functions and their roles in diseases.


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