Neuroplastin 65 mediates cognitive functions via excitatory/inhibitory synapse imbalance and ERK signal pathway

Amuti, Siyiti; Tang, Yuchun; Wu, Shuang; Liu, Lifen; Huang, Liang; Zhang, Haibo; Li, Huanhuan; Fen, Jiang; Wang, Geying; Liu, Xiaoqing; Yuan, Qionglan

doi:10.1016/j.nlm.2015.11.020

Cited by 26 publications

(49 citation statements)

References 47 publications

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“…Integrin exhibits increased resistance to glutamate-induced apoptosis (Gary and Mattson, 2001). Our previous studies have shown that Np65 gene deletion does not affect locomotor activity and brain framework of organization in adult mice (Amuti et al, 2016). In addition, we showed that peptides derived from NP Ig1 or Ig2 significantly increased the survival of primary cerebellar granule neurons induced to undergo apoptosis by low KCl in the media (Owczarek et al, 2011), suggesting that Np65 protects neurons against apoptosis in vitro .…”

Section: Discussionmentioning

confidence: 93%

“…Np65 gene deletion did not affect locomotor activity of mice (Amuti et al, 2016). Before stroke, both type mice exhibited normal motor movement, sensory, reflex, and balance, the scores were 0.…”

Section: Resultsmentioning

confidence: 99%

“…Generation and characterization of Np65 knock-out mice (KO) and their WT littermates were described in our lab (Amuti et al, 2016). In brief, C57BL/6J Np65 heterozygotes (Np65 +/− ) mice were backcrossed to C57BL/6J mice (Slac Laboratory Animal Center, Shanghai) for at least five generations and resulting offspring were subsequently bred to generate homozygous offspring.…”

Section: Methodsmentioning

confidence: 99%

“…In brief, C57BL/6J Np65 heterozygotes (Np65 +/− ) mice were backcrossed to C57BL/6J mice (Slac Laboratory Animal Center, Shanghai) for at least five generations and resulting offspring were subsequently bred to generate homozygous offspring. Genotyping of the offspring was performed by PCR of tail DNA extracts and by Western blot of Np65 (Amuti et al, 2016). …”

Section: Methodsmentioning

confidence: 99%

“…In addition, our previous studies have found that Np65 may be involved in modulation of neuritogenesis in vitro (Owczarek et al, 2011). More recently, we found that Np65 knock-out mice exhibit enhanced hippocampus-dependent learning and memory and anxiety-like behaviors (Amuti et al, 2016). …”

Section: Introductionmentioning

confidence: 92%

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Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity

Zhan

Zhang

et al. 2017

Front. Cell. Neurosci.

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Cell adhesion molecules (CAMs) are involved in synaptic plasticity and neuronal survival in the adult brain. Neuroplastin 65 (Np65), one member of the immunoglobulin superfamily of CAMs, is brain-specific and highly expressed in rodent forebrain. The roles of Np65 in synaptic plasticity have been confirmed, however, whether Np65 affects neuronal survival remains unknown. To address this gap, we generated, to our knowledge, the first Np65 knockout (KO) mice. By occluding middle cerebral artery to perform ischemic stroke model, we showed that Np65 KO mice exhibited more severe neurological deficits and larger infarction volume measured by TTC staining and more apoptotic cells confirmed by TUNEL staining compared to wild type (WT) mice. Besides, western blot analysis showed that the vesicular glutamate transporter-1(VGluT1), and N-Methyl D-Aspartate receptors, including NR1, NR2A, and NR2B were significantly increased in Np65 KO mice compared with WT mice. In contrast, vesicular gamma amino butyric acid transporter (VGAT) levels were unchanged in two genotypes after stroke. Additionally, phosphorylated-extracellular signal-regulated kinase 1/2 levels were significantly increased in Np65 KO mice compared with WT mice after stroke. Together, these results suggest that Np65 KO mice may be more susceptible to ischemic events in the brain.

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Section: Discussionmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

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Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity

Zhan

Zhang

et al. 2017

Front. Cell. Neurosci.

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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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Autonomic behavioral impairment induced by simazine exposure during early life of male mouse is mediated by Lmx1a/Wnt1 pathway

Jiang

et al. 2021

Environmental Toxicology

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Simazine is a widely used herbicide and known as an environmental estrogen. Multiple studies have proved simazine can induced the degeneration of dopaminergic neuron resulting in a degenerative disease-like syndrome. Herein, we explored the neurotoxicity of simazine on the dopaminergic nervous system of embryos and weaned offspring during the maternal gestation period or the maternal gestation and lactation periods. We found that simazine disturbed the crucial components expression involved in Lmx1a/Wnt1 pathway of dopaminergic neuron in embryonic and weaned offspring. Furthermore, morphological and behavioral tests performed on weaned male offspring treated by simazine suggested that the grip strength, autonomic exploring, and the space sense ability were weakened, as well as the pathological damage of dopaminergic neuron was clearly observed. But, the same neurotoxicity of simazine is less significantly observed in female offspring. Our findings will provide reliable reference for the determination of environmental limits and new insight into the pathogenesis of nonfamilial neurodegenerative diseases related to environmental risk factors.

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Neuroplastin 65 mediates cognitive functions via excitatory/inhibitory synapse imbalance and ERK signal pathway

Cited by 26 publications

References 47 publications

Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity

Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity

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

Autonomic behavioral impairment induced by simazine exposure during early life of male mouse is mediated by Lmx1a/Wnt1 pathway

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