Possible glutamatergic and lipid signalling mechanisms in ECT-induced retrograde amnesia: Experimental evidence for involvement of COX-2, and review of literature

Andrade, Chittaranjan; Singh, Namrata; Thyagarajan, Shivashanmugam; Nandakumar, Natarajan; Rao, N. Sanjay Kumar; Chandra, J. Suresh

doi:10.1016/j.jpsychires.2007.08.009

Cited by 33 publications

(24 citation statements)

References 70 publications

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“…ECS-induced amnesia arises from pathologically upregulating the glutamatergic system and its excitotoxicity [23]. A seizure can remove the blockage of magnesium on the NMDA receptor, resulting in an influx of cations and water into the cell, oxidative stress, and saturation of hippocampal long-term potentiation [6].…”

Section: Discussionmentioning

confidence: 99%

Propofol protects against impairment of learning-memory and imbalance of hippocampal Glu/GABA induced by electroconvulsive shock in depressed rats

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Propofol protects against impairment of learning-memory and imbalance of hippocampal Glu/GABA induced by electroconvulsive shock in depressed rats

et al. 2011

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“…Recently, one group suggested involvement of COX-2 in ECSinduced retrograde amnesia. 39) Administration of five ECSs resulted in significant retrograde amnesia on the step-down passive avoidance task in rats. This memory impairment was significantly protected by chronic treatment with celecoxib, a COX-2 inhibitor, suggesting that COX-2-dependent prostanoids are involved in ECS-induced memory impairment.…”

Section: Possible Roles Of Ecs-induced Cox-2 In Hippocampusmentioning

confidence: 97%

Exploration of New Molecular Mechanisms for Antidepressant Actions of Electroconvulsive Seizure

Segi-Nishida

2011

Biological & Pharmaceutical Bulletin

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Electroconvulsive seizure (ECS) therapy is a clinically proven treatment for depression and is often effective even in patients resistant to chemical antidepressants. However, the molecular mechanisms underlying the therapeutic efficacy of ECS are not fully understood. Here, I review studies that show molecular, cellular, and behavioral changes by ECS treatment, and discuss the functions of ECS to underlie the action of antidepressant effects. In hippocampus, these changes cover gene induction, increased adult neurogenesis, and electrophysiological reactivity. Especially, the role of vascular endothelial growth factor (VEGF) in neurogenesis is discussed. Among other gene expression changes in hippocampus, a role of cyclooxygenase (COX)-2, an inducible type of the rate-limiting enzyme of prostanoid synthesis, is focused. ECS-induced changes in other brain regions such as prefrontal cortex and hypothalamus, and ECS-induced behavioral changes are also reviewed. Understanding the molecular, cellular, and behavioral changes by ECS will provide a new view to find potential targets for novel antidepressant design that are highlighted by these findings.

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“…Controversially, recent studies have shown that elevated CSF Nrgn levels are associated with increased severity of cognitive decline (Hellwig et al, 2015; Janelidze et al, 2016; Kester et al, 2015; Portelius et al, 2015). Increased Nrgn phosphorylation has also been associated with memory impairments (Andrade et al, 2008; Kim et al, 2010; Severino et al, 2011). Although the role of increased Nrgn phosphorylation in relation to cognitive function requires further investigation, our results demonstrate that dual-LPS administration decreases cytosolic and synaptosomal phosphorylation of NFAT1 in the mPFC.…”

Section: Discussionmentioning

confidence: 99%

LPS-induced cortical kynurenic acid and neurogranin-NFAT signaling is associated with deficits in stimulus processing during Pavlovian conditioning

Oliveros

Wininger

Larsson

et al. 2017

Journal of Neuroimmunology

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The N-Methyl-D-Aspartate receptor (NMDAR) antagonist kynurenic acid (KYNA) and the post-synaptic calmodulin binding protein neurogranin (Nrgn) have been implicated in neurological and neuropsychiatric conditions including Alzheimer's disease and schizophrenia. This study indicates that systemic dual-lipopolysaccharide (LPS) injections increases KYNA in the medial prefrontal cortex (mPFC), which is accompanied with increased phosphorylation of nuclear factor kappa chain of activated B cells (NFκB) and activation of the nuclear factor of activated T- cells (NFAT). Our results also indicate that dual-LPS increases Nrgn phosphorylation and concomitantly reduces phosphorylation of calmodulin kinase-I I (CaMKII). We confirmed that systemic blockade of kynurenine-3 monooxygenase in conjunction with kynurenine administration results in significant increases in Nrgn phosphorylation and a significant reduction of CaMKII phosphorylation in the mPFC. Consequently dual-LPS administration induced significant impairments in stimulus processing during Pavlovian conditioning. Taken together, our study indicates that elevations in KYNA in the mPFC can directly regulate NMDA-Nrgn-CaMKII signaling, suggesting that neuroinflammatory conditions affecting this pathway may be associated with cognitive dysfunction.

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Possible glutamatergic and lipid signalling mechanisms in ECT-induced retrograde amnesia: Experimental evidence for involvement of COX-2, and review of literature

Cited by 33 publications

References 70 publications

Propofol protects against impairment of learning-memory and imbalance of hippocampal Glu/GABA induced by electroconvulsive shock in depressed rats

Propofol protects against impairment of learning-memory and imbalance of hippocampal Glu/GABA induced by electroconvulsive shock in depressed rats

Exploration of New Molecular Mechanisms for Antidepressant Actions of Electroconvulsive Seizure

LPS-induced cortical kynurenic acid and neurogranin-NFAT signaling is associated with deficits in stimulus processing during Pavlovian conditioning

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