Mitochondrial Superoxide Production and MnSOD Activity after Exposure to Agonist and Antagonists of Ionotropic Glutamate Receptors in Hippocampus

2005 ◽  
Vol 1048 (1) ◽  
pp. 363-365 ◽  
Author(s):  
LIDIJA RADENOVIĆ ◽  
VESNA SELAKOVIĆ ◽  
GORDANA KARTELIJA
2015 ◽  
Vol 67 (2) ◽  
pp. 741-741
Author(s):  
E Editorial

This is a notice of retraction of the article: Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic glutamate receptors in rat brain, published in the Archives of Biological Sciences in 2005, Vol. 57, Issue 1. The Editor-in-Chief has been informed that this paper plagiarizes an earlier paper: Radenovic L, Selakovic V, Kartelija G, Todorovic N, Nedeljkovic M. Differential effects of NMDA and AMPA/kainate receptor antagonists on superoxide production and MnSOD activity in rat brain following intrahippocampal injection. Brain Res Bull, 2004, 64(1):85-93. This claim is correct and almost the entire paper is a verbatim copy of the earlier one. After confirmation of this fact, the Editor-in-Chief of the Archives of Biological Sciences has decided to retract the paper immediately. We apologize to the readers of the journal that it took so many years to notice this error and to retract the paper. We request readers of the journal to directly get in touch with the editorial office and the editors of the journal for similar cases in the future, so that they can be handled promptly. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0501001R">10.2298/ABS0501001R</a></b></u>


2021 ◽  
pp. 108631
Author(s):  
David Stroebel ◽  
Laetitia Mony ◽  
Pierre Paoletti

Author(s):  
Luukkonen Jukka ◽  
Höytö Anne ◽  
Sokka Miiko ◽  
Syväoja Juhani ◽  
Juutilainen Jukka ◽  
...  

AbstractIonizing radiation has been shown to cause induced genomic instability (IGI), which is defined as a persistently increased rate of genomic damage in the progeny of the exposed cells. In this study, IGI was investigated by exposing human SH-SY5Y neuroblastoma cells to hydroxyurea and zeocin, two chemicals mimicking different DNA-damaging effects of ionizing radiation. The aim was to explore whether IGI was associated with persistent mitochondrial dysfunction. Changes to mitochondrial function were assessed by analyzing mitochondrial superoxide production, mitochondrial membrane potential, and mitochondrial activity. The formation of micronuclei was used to determine immediate genetic damage and IGI. Measurements were performed either immediately, 8 days, or 15 days following exposure. Both hydroxyurea and zeocin increased mitochondrial superoxide production and affected mitochondrial activity immediately after exposure, and mitochondrial membrane potential was affected by zeocin, but no persistent changes in mitochondrial function were observed. IGI became manifested 15 days after exposure in hydroxyurea-exposed cells. In conclusion, immediate responses in mitochondrial function did not cause persistent dysfunction of mitochondria, and this dysfunction was not required for IGI in human neuroblastoma cells.


Author(s):  
Yukari Maeno ◽  
Yuichi Kotaki ◽  
Ryuta Terada ◽  
Masafumi Hidaka ◽  
Yuko Cho ◽  
...  

Domoic acid (1, DA), a member of the natural kainoid family, is a potent agonist of ionotropic glutamate receptors in the central nervous system. The chemical synthesis of DA and...


Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 77
Author(s):  
Fabrizio Gardoni ◽  
Jennifer Stanic ◽  
Diego Scheggia ◽  
Alberto Benussi ◽  
Barbara Borroni ◽  
...  

The role of autoimmunity in central nervous system (CNS) disorders is rapidly expanding. In the last twenty years, different types of autoantibodies targeting subunits of ionotropic glutamate receptors have been found in a variety of patients affected by brain disorders. Several of these antibodies are directed against NMDA receptors (NMDAR), mostly in autoimmune encephalitis, whereas a growing field of research has identified antibodies against AMPA receptor (AMPAR) subunits in patients with different types of epilepsy or frontotemporal dementia. Several in vitro and in vivo studies performed in the last decade have dramatically improved our understanding of the molecular and functional effects induced by both NMDAR and AMPAR autoantibodies at the excitatory glutamatergic synapse and, consequently, their possible role in the onset of clinical symptoms. In particular, the method by which autoantibodies can modulate the localization at synapses of specific target subunits leading to functional impairments and behavioral alterations has been well addressed in animal studies. Overall, these preclinical studies have opened new avenues for the development of novel pharmacological treatments specifically targeting the synaptic activation of ionotropic glutamate receptors.


2013 ◽  
Vol 104 (2) ◽  
pp. 272a
Author(s):  
Christel B. Jensen ◽  
Niels G. Nørager ◽  
Anders S. Kristensen ◽  
Kristian Strømgaard

2014 ◽  
Vol 75 ◽  
pp. 151-158 ◽  
Author(s):  
Andrea Pinto ◽  
Lucia Tamborini ◽  
Federica Mastronardi ◽  
Roberta Ettari ◽  
Yeliz Safoz ◽  
...  

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