Regulation of emotional memory by hydrogen sulfide: role of GluN2B‐containing <scp>NMDA</scp> receptor in the amygdala

Wang, Canming; Yang, Yuan-Jian; Zhang, Jie-Ting; Liu, Jue; Guan, Xin-Lei; Li, Mingxing; Lu, Haifeng; Wu, Pengfei; Chen, Jianguo; Wang, Fang

doi:10.1111/jnc.12961

Cited by 22 publications

(22 citation statements)

References 44 publications

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“…The dose of ifenprodil used in this study (1 μg in 0.3 μl per hemisphere) is comparable to doses of ifenprodil used by other groups to investigate how antagonizing GluN2B-containing NMDA receptors affects neuronal physiology and behaviors mediated by certain brain regions [60, 99, 100]. This dose of ifenprodil has the potential to cause off-target effects, however.…”

Section: Discussionmentioning

confidence: 98%

Ifenprodil infusion in agranular insular cortex alters social behavior and vocalizations in rats exposed to moderate levels of ethanol during prenatal development

Bird

Barto

Magcalas

et al. 2017

Behavioural Brain Research

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Moderate exposure to alcohol during development leads to subtle neurobiological and behavioral effects classified under the umbrella term fetal alcohol spectrum disorders (FASDs). Alterations in social behaviors are a frequently observed consequence of maternal drinking, as children with FASDs display inappropriate aggressive behaviors and altered responses to social cues. Rodent models of FASDs mimic the behavioral alterations seen in humans, with rats exposed to ethanol during development displaying increased aggressive behaviors, decreased social investigation, and altered play behavior. Work from our laboratory has observed increased wrestling behavior in adult male rats following prenatal alcohol exposure (PAE), and increased expression of GluN2B-containing NMDA receptors in the agranular insular cortex (AIC). This study was undertaken to determine if ifenprodil, a GluN2B preferring negative allosteric modulator, has a significant effect on social behaviors in PAE rats. Using a voluntary ethanol exposure paradigm, rat dams were allowed to drink a saccharin-sweetened solution of either 0% or 5% ethanol throughout gestation. Offspring at 6–8 months of age were implanted with cannulae into AIC. Animals were isolated for 24 hours before ifenprodil or vehicle was infused into AIC, and after 15 minutes they were recorded in a social interaction chamber. Ifenprodil treatment altered aspects of wrestling, social investigatory behaviors, and ultrasonic vocalizations in rats exposed to ethanol during development that were not observed in control animals. These data indicate that GluN2B-containing NMDA receptors in AIC play a role in social behaviors and may underlie alterations in behavior and vocalizations observed in PAE animals.

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Section: Discussionmentioning

confidence: 98%

Ifenprodil infusion in agranular insular cortex alters social behavior and vocalizations in rats exposed to moderate levels of ethanol during prenatal development

Bird

Barto

Magcalas

et al. 2017

Behavioural Brain Research

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“…A plethora of evidence suggest that H 2 S regulates NMDA-R in many physiological and pathophysiological conditions [42; 43; 44; 45]. In the kidney, NMDA-R expresses abundantly in several tissue compartments including outer medulla, cortical brush boarder membrane and glomeruli [46].…”

Section: Discussionmentioning

confidence: 99%

MMP-9- and NMDA receptor-mediated mechanism of diabetic renovascular remodeling and kidney dysfunction: Hydrogen sulfide is a key modulator

2015

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Previously we reported that matrix metalloproteinase-9 (MMP-9) plays an important role in extracellular matrix (ECM) remodeling in diabetic kidney. Induction of NMDA-R and dysregulation of connexins (Cxs) were also observed. We concluded that this was due to decreased H2S production by down regulation of CBS and CSE enzymes. However, the potential role of H2S to mitigate ECM dysregulation and renal dysfunction was not clearly understood. The present study was undertaken to determine whether H2S supplementation reduces MMP-9-induced ECM remodeling and dysfunction in diabetic kidney. Wild type (C57BL/6J), diabetic (Akita, C57BL/6J-Ins2Akita), MMP-9 knockout (MMP-9−/− , M9KO) and double KO of Akita/MMP-9−/− (DKO) mice were treated without or with 0.05 g/L of NaHS (as a source of H2S) in drinking water for 30 days. Decreased tissue production and plasma content of H2S in Akita mice were ameliorated with H2S supplementation. Dysregulated expression of MMP-9, CBS, CSE, NMDA-R1 and Cxs-40, -43 were also normalized in Akita mice treated with H2S. In addition, increased renovascular resistive index (RI), ECM deposition, plasma creatinine, and diminished renal vascular density and cortical blood flow in Akita mice were normalized with H2S treatment. We conclude that diminished H2S production in renal tissue and plasma levels in diabetes mediates adverse renal remodeling, and H2S therapy improves renal function through MMP-9- and NMDA-R1-mediated pathway.

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“…The cue‐fear conditioning experiment was performed as described previously (Wang et al ., ; Li et al ., ; Wang et al ., ). The experiment was conducted over 3 days, conditioning day, reactivation day and testing day.…”

Section: Methodsmentioning

confidence: 97%

Propranolol decreases retention of fear memory by modulating the stability of surface glutamate receptor GluA1 subunits in the lateral amygdala

Zhou

Luo

Zhang

et al. 2015

British J Pharmacology

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BACKGROUND AND PURPOSEPosttraumatic stress disorder (PTSD) is a mental disorder with enhanced retention of fear memory and has profound impact on quality of life for millions of people worldwide. The β-adrenoceptor antagonist propranolol has been used in preclinical and clinical studies for the treatment of PTSD, but the mechanisms underlying its potential efficacy on fear memory retention remain to be elucidated. EXPERIMENTAL APPROACHWe investigated the action of propranolol on the retention of conditioned fear memory, the surface expression of glutamate receptor GluA1 subunits of AMPA receptors and synaptic adaptation in the lateral amygdala (LA) of rats. KEY RESULTSPropranolol attenuated reactivation-induced strengthening of fear retention while reducing enhanced surface expression of GluA1 subunits and restoring the impaired long-term depression in LA. These effects of propranolol were mediated by antagonizing reactivation-induced enhancement of adrenergic signalling, which activates PKA and calcium/calmodulin-dependent protein kinase II and then regulates the trafficking of AMPA receptors via phosphorylation of GluA1 subunits at the C-terminus. Both i.p. injection and intra-amygdala infusion of propranolol attenuated reactivation-induced enhancement of fear retention. CONCLUSIONS AND IMPLICATIONSReactivation strengthens fear retention by increasing the level of noradrenaline and promotes the surface expression of GluA1 subunits and the excitatory synaptic transmission in LA. These findings uncover one mechanism underlying the efficiency of propranolol on retention of fear memories and suggest that β-adrenoceptor antagonists, which act centrally, may be more suitable for the treatment of PTSD. Abbreviations

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Regulation of emotional memory by hydrogen sulfide: role of GluN2B‐containing NMDA receptor in the amygdala

Cited by 22 publications

References 44 publications

Ifenprodil infusion in agranular insular cortex alters social behavior and vocalizations in rats exposed to moderate levels of ethanol during prenatal development

Ifenprodil infusion in agranular insular cortex alters social behavior and vocalizations in rats exposed to moderate levels of ethanol during prenatal development

MMP-9- and NMDA receptor-mediated mechanism of diabetic renovascular remodeling and kidney dysfunction: Hydrogen sulfide is a key modulator

Propranolol decreases retention of fear memory by modulating the stability of surface glutamate receptor GluA1 subunits in the lateral amygdala

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