αCaMKII in the lateral amygdala mediates PTSD-Like behaviors and NMDAR-Dependent LTD

An, Shuming; Wang, Jiayue; Zhang, Xuliang; Duan, Yi‐Shi; Xu, Yi-Qiong; Lv, Junyan; Wang, Dasheng; Zhang, Huan; Richter‐Levin, Gal; Klavir, Oded; Yu, Bo; Cao, Xiaohua

doi:10.1016/j.ynstr.2021.100359

Cited by 13 publications

(10 citation statements)

References 88 publications

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“…These results indicate that UWT stress may lead to widespread increase of αCaMKII activity in the hippocampus, and that αCaMKII may be important in PTSD. Moreover, our previous study already showed that UWT rats also exhibited increased αCaMKII activity in the amygdala, and artificially up-regulated αCaMKII expression in the amygdala impaired LTD, fear extinction, and induced PTSD-like behavior in mice [21]. In addition, Wu et al observed that genistein (tyrosine kinase inhibitor) could improve PTSD-like behaviors by reversing αCaMKII activity in the amygdala of electric shock model mice [30].…”

Section: Discussionmentioning

confidence: 95%

“…At the synaptic level, LTD has been implicated in fear extinction [21]. For example, studies have reported that both Schaffer collateral pathway LTD and fear extinction were impaired in electric shock model rats [23].…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that hippocampal function is sub-region specific, and different sub-regions play different roles in cognition and emotion [14,15]. Moreover, LTD has been implicated in fear extinction [21]. Since UWT rats exhibited impaired fear extinction, we detected LTD in different sub-regions and pathways in the hippocampus of rats after UWT training by using field potential recordings.…”

Section: Uwt Rats Exhibited Impaired Ltd In Different Hippocampal Sub...mentioning

confidence: 90%

“…An inability for fear extinction is a major cause of PTSD; long-term depression (LTD) has been implicated in fear extinction [21]. An impairment of Schaffer collateral pathway LTD has been reported in immobilization on board model rats (a PTSD model) [22].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The neural mechanism of the different sub-regions of hippocampus involved in post-traumatic stress disorder

Zuo¹,

Zhou²,

Zhou³

et al. 2022

Stress and Brain

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post-traumatic stress disorder (PTSD), under water trauma (UWT) model rats, long-term depression, alpha calcium/calmodulin-dependent protein kinase II (αCaMKII) Post-traumatic stress disorder (PTSD) patients have severe fear extinction disorder, but the underlying molecular and neurobiological mechanisms are still unknown. The hippocampus has sub-regional specific functions, however, their involvement in PTSD is unclear. In this study, we used under water trauma (UWT) model rats which exhibit multiple core PTSD symptoms, including anxiety, depression, and impaired fear extinction. In the dorsal or ventral hippocampus, we found that long-term depression at Schaffer collateral and medial perforant pathway were impaired in UWT model rats. Moreover, although the expression levels of ionotropic glutamate receptors including NR2A, NR2B, GluA1, and GluA2 were normal, the activity of alpha calcium/calmodulin-dependent protein kinase II (αCaMKII) significantly increased in both the dorsal and ventral hippocampus of UWT model rats. These findings reveal similar abnormalities in synaptic plasticity and αCaMKII activity in different hippocampal sub-regions of UWT rats. Our results shed light on the regionspecific role of the hippocampus in PTSD and provide a theoretical basis for the development of specific treatments for PTSD.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Uwt Rats Exhibited Impaired Ltd In Different Hippocampal Sub...mentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The neural mechanism of the different sub-regions of hippocampus involved in post-traumatic stress disorder

Zuo¹,

Zhou²,

Zhou³

et al. 2022

Stress and Brain

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show abstract

“…While GWAS identified GluA1 dysfunction as a risk factor for schizophrenia [12], molecular and pharmacological studies over the past decade have linked GluA1 to depression, anxiety, stress-related behavior, and Alzheimer's disease [71][72][73][74]. Interestingly, the levels of GluA1 expression and phosphorylation appear to be important for these neurological conditions [71,73,75,76]. In the future, it would be interesting to determine whether the phosphorylation state of GluA1 is modified by its interaction with Np65 or by the loss of neuroplastin.…”

Section: Figurementioning

confidence: 99%

Neuroplastin in Neuropsychiatric Diseases

Lin

Liang

Herrera-Molina

et al. 2021

Genes

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Molecular mechanisms underlying neuropsychiatric and neurodegenerative diseases are insufficiently elucidated. A detailed understanding of these mechanisms may help to further improve medical intervention. Recently, intellectual abilities, creativity, and amnesia have been associated with neuroplastin, a cell recognition glycoprotein of the immunoglobulin superfamily that participates in synapse formation and function and calcium signaling. Data from animal models suggest a role for neuroplastin in pathways affected in neuropsychiatric and neurodegenerative diseases. Neuroplastin loss or disruption of molecular pathways related to neuronal processes has been linked to various neurological diseases, including dementia, schizophrenia, and Alzheimer’s disease. Here, we review the molecular features of the cell recognition molecule neuroplastin, and its binding partners, which are related to neurological processes and involved in learning and memory. The emerging functions of neuroplastin may have implications for the treatment of diseases, particularly those of the nervous system.

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Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

Doğanyiğit,

Okan,

Yılmaz

et al. 2024

Synapse

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Epileptic seizures are seen as a result of changing excitability balance depending on the deterioration in synaptic plasticity in the brain. Neuroplastin, and its related molecules which are known to play a role in synaptic plasticity, neurotransmitter activities that provide balance of excitability and, different neurological diseases, have not been studied before in epilepsy.In this study, a total of 34 Sprague–Dawley male and female rats, 2 months old, weighing 250–300 g were used. The epilepsy model in rats was made via pentylenetetrazole (PTZ). After the completion of the experimental procedure, the brain tissue of the rats were taken and the histopathological changes in the hippocampus and cortex parts and the brain stem were investigated, as well as the immunoreactivity of the proteins related to the immunohistochemical methods.As a result of the histopathological evaluation, it was determined that neuron degeneration and the number of dilated blood vessels in the hippocampus, frontal cortex, and brain stem were higher in the PTZ status epilepticus (SE) groups than in the control groups. It was observed that neuroplastin and related proteins TNF receptor‐associated factor 6 (TRAF6), Gamma amino butyric acid type A receptors [(GABA(A)], and plasma membrane Ca2+ ATPase (PMCA) protein immunoreactivity levels increased especially in the male hippocampus, and only AMPA receptor subunit type 1 (GluA1) immunoreactivity decreased, unlike other proteins.We believe this may be caused by a problem in the mechanisms regulating the interaction of neuroplastin and GluA1 and may cause problems in synaptic plasticity in the experimental epilepsy model. It may be useful to elucidate this mechanism and target GluA1 when determining treatment strategies.

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αCaMKII in the lateral amygdala mediates PTSD-Like behaviors and NMDAR-Dependent LTD

Cited by 13 publications

References 88 publications

The neural mechanism of the different sub-regions of hippocampus involved in post-traumatic stress disorder

The neural mechanism of the different sub-regions of hippocampus involved in post-traumatic stress disorder

Neuroplastin in Neuropsychiatric Diseases

Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

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