MGE-derived nNOS + interneurons promote fear acquisition in nNOS −/− mice

Zhou, Lin; Yuan, Hong‐Jin; Cao, Bo; Kong, Chengcheng; Fang, Yuan; Li, Jun; Ni, Huan‐Yu; Wu, Hai‐Yin; Chang, Lei; Liu, Yan; Luo, Chunxia

doi:10.1016/j.bbrc.2017.09.158

Cited by 2 publications

(3 citation statements)

References 41 publications

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“…Additionally, the administration of the NO donor molsidomine to nNOS KO mice improved the previous deficits in short- and long-term contextual fear memory [ 62 ]. Interestingly, when nNOS+ interneurons were transplanted in the dentate gyrus of nNOS KO mice, the acquisition of fear memory was restored, indicating the necessity of nNOS+ neurons in learning, in this particular case of an aversive memory [ 63 ]. Conversely, iNOS KO mice, which might have a compensatory increase in nNOS activity in the brain, besides not presenting differences in contextual fear conditioning expression, have deficits in fear extinction when compared to WT animals [ 64 ].…”

Section: No Involvement In Learned Fearmentioning

confidence: 99%

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Fronza,

Ferreira,

Pavan-Silva

et al. 2023

Molecules

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Post-traumatic stress disorder (PTSD) is a psychiatric condition characterized by persistent fear responses and altered neurotransmitter functioning due to traumatic experiences. Stress predominantly affects glutamate, a neurotransmitter crucial for synaptic plasticity and memory formation. Activation of the N-Methyl-D-Aspartate glutamate receptors (NMDAR) can trigger the formation of a complex comprising postsynaptic density protein-95 (PSD95), the neuronal nitric oxide synthase (nNOS), and its adaptor protein (NOS1AP). This complex is pivotal in activating nNOS and nitric oxide (NO) production, which, in turn, activates downstream pathways that modulate neuronal signaling, including synaptic plasticity/transmission, inflammation, and cell death. The involvement of nNOS and NOS1AP in the susceptibility of PTSD and its comorbidities has been widely shown. Therefore, understanding the interplay between stress, fear, and NO is essential for comprehending the maintenance and progression of PTSD, since NO is involved in fear acquisition and extinction processes. Moreover, NO induces post-translational modifications (PTMs), including S-nitrosylation and nitration, which alter protein function and structure for intracellular signaling. Although evidence suggests that NO influences synaptic plasticity and memory processing, the specific role of PTMs in the pathophysiology of PTSD remains unclear. This review highlights pathways modulated by NO that could be relevant to stress and PTSD.

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Section: No Involvement In Learned Fearmentioning

confidence: 99%

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Fronza,

Ferreira,

Pavan-Silva

et al. 2023

Molecules

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“…A number of studies have shown that transfer of memory from the stable state to the labile due to reactivation requires involvement of nitric oxide. Its role in the mechanisms of synaptic plasticity, learning, and memory have repeatedly been described [Antonov et al, 2007;Lisboa et al, 2015;Bradley and Steinert, 2016;Chen et al, 2016;Hott et al, 2017;Li et al, 2017;Zhang et al, 2017;Cai et al, 2018;Dyer et al, 2019;Noriega-Prieto et al, 2019;Bingor et al, 2020;Song et al, 2020]. More recent studies in terrestrial mollusks showed that nitric oxide is needed for destabilization (labilization) of contextual memories and triggering the process of reconsolidation [Balaban et al, 2014].…”

mentioning

confidence: 98%

“…Discussion. There is currently extensive evidence for the involvement of nitric oxide in synaptic plasticity, learning, and memory [Antonov et al, 2007;Lisboa et al, 2015;Bradley and Steinert, 2016;Chen et al, 2016;Hott et al, 2017;Li et al, 2017;Zhang et al, 2017;Cai et al, 2018;Dyer et al, 2019;Noriega-Prieto et al, 2019;Bingor et al, 2020;Song et al, 2020]. However, little is known of the interaction between nitric oxide production and the process of memory destabilization on reminding.…”

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confidence: 99%

Nitric Oxide Is Required for Labilization (destabilization) of Contextual Memory in Rats

Vinarskaya

Zuzina

Balaban

2021

Neurosci Behav Physi

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It is well known that nitric oxide (NO) is involved in forming signal memory for stimulation of different modalities. We studied the involvement of nitric oxide in processes of the reconsolidation (repeated consolidation of a long-term memory on reminding) of conditioned refl ex contextual fear memory in rats. After a single training session, animals demonstrated signifi cant increases in freezing on presentation of the conditioned context. Reactivation of this memory on the background of blockade of de novo protein synthesis with cycloheximide led to a signifi cant decrease in freezing time in the conditioned context in rats. Administration of the selective neuronal NO synthase blocker 3-bromo-7-indazole in conditions of memory reactivation on the background of protein synthesis blockade prevented weakening of conditioned refl ex freezing reactions, as demonstrated by subsequent testing of animals in the conditioned context. In addition, administration of 3-bromo-7-indazole without reactivation did not elicit signifi cant changes in measures of conditioned refl ex freezing in rats. These results suggest that nitric oxide is involved in the labilization of conditioned refl ex contextual fear memory on reminding, and is thus a necessary component of the triggering of the reconsolidation process.

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MGE-derived nNOS + interneurons promote fear acquisition in nNOS −/− mice

Cited by 2 publications

References 41 publications

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Nitric Oxide Is Required for Labilization (destabilization) of Contextual Memory in Rats

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