Improvement of synaptic plasticity by nanoparticles and the related mechanisms: Applications and prospects

Chen, Aijie; Kang, Youjeong; Liu, Jia; Wu, Junrong; Feng, Xiaoli; Wang, Menglei; Wang, Ruolan; Lai, Xuan; Shao, Longquan

doi:10.1016/j.jconrel.2022.04.049

Cited by 4 publications

(3 citation statements)

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“…Previous studies have found that neuroinflammation is accompanied by a large release of inflammatory factors, which could affect the synaptic transmission of neurons and lead to neuronal damage. [11,28] To evaluate whether ZnO NPs cause neuroinflammation, we performed immunohistochemical staining of brain tissue in the GC region. We found that TNF-𝛼 and IL-1𝛽 (brown) were significantly increased in the high-, medium-, and low-dose groups, suggesting that neuroinflammation occurred in the GC region (Figure 4A; Figure S8, Supporting Information).…”

Section: Transport Of Zno Nps Into the Brain Induced Neuroinflammatio...mentioning

confidence: 99%

“…[9,10] It involves the expression of presynaptic membrane and postsynaptic proteins, the release of presynaptic neurotransmitters, and the distribution of postsynaptic receptors. [11] Synaptic transmission is a complex physiological process that can be affected by many factors. [12,13] Would ZnO NPs affect synaptic transmission and subsequently influence neuronal functions?…”

Section: Introductionmentioning

confidence: 99%

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Tongue−Brain‐Transported ZnO Nanoparticles Induce Abnormal Taste Perception

Chen

Wang

Kang

et al. 2023

Adv Healthcare Materials

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Nanoparticles (NPs) can be transported to the brain, especially through nerves, because of their small size and high biological activity. Previous studies confirmed that zinc oxide (ZnO) NPs can enter the brain through the tongue−brain pathway, but it is unclear whether they will further affect synaptic transmission and brain perception. In this study, it is found that tongue−brain‐transported ZnO NPs can cause a decrease in taste sensitivity and taste aversion learning ability, indicating abnormal taste perception. Moreover, the release of miniature excitatory postsynaptic currents, the frequency of action potential release, and the expression of c‐fos are decreased, suggesting that the synaptic transmission is reduced. To further explore the mechanism, protein chip detection of inflammatory factors is carried out and it is found that neuroinflammation occurs. Importantly, it is found that neuroinflammation originated from neurons. The JAK‐STAT signaling pathway is activated, which inhibits the Neurexin1‐PSD95‐Neurologigin1 pathway and c‐fos expression. Blocking the activation of the JAK‐STAT pathway prevents neuroinflammation and the reduction in Neurexin1‐PSD95‐Neurologigin1. These results indicate that ZnO NPs can be transported by the tongue−brain pathway and lead to abnormal taste perception by neuroinflammation‐induced deficits in synaptic transmission. The study reveals the influence of ZnO NPs on neuronal function and provides a novel mechanism.

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Section: Transport Of Zno Nps Into the Brain Induced Neuroinflammatio...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tongue−Brain‐Transported ZnO Nanoparticles Induce Abnormal Taste Perception

Chen

Wang

Kang

et al. 2023

Adv Healthcare Materials

Self Cite

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“…Nicotine (Nic) is a principal bioactive ingredient in cigarettes and the component most associated with tobacco dependence ( Tanner et al, 2015 ; Xiao et al, 2020 ). The development and persistence of tobacco dependence are due to the reward effect produced by activating nicotine acetylcholine receptors (nAChRs) in the mesolimbic reward circuitry ( Tapper et al, 2004 ; Changeux, 2010 ; Henderson et al, 2017 ; Chen et al, 2022 ). In addition to its strong addictive potential, extensive studies showed that Nic is a potential drug for the amelioration of ulcerative colitis, Alzheimer’s disease, and Parkinson’s disease ( Quik et al, 2012 ; Quik et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetic and pharmacodynamic studies of nicotine in rat brain: a simultaneous investigation of nicotine metabolites and the release of neurotransmitters in vivo

Guo,

Mao,

Zhang

et al. 2023

Front. Chem.

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Introduction: The body’s ability to metabolize nicotine and the disposition of nicotine in the brain are important determinants of its exposure. Limited knowledge about the near real-time changes of neurochemicals during the brain nicotine metabolic process hinders the recognition of its multiple neuropharmacological effects.Methods: An online microdialysis coupled with UHPLC-HRMS/MS method for the in vivo multi-analysis of nicotine metabolites and several neurotransmitters in rat brain was developed. Whether the systemic modulation of metabolic enzyme CYP2B would modulate nicotine pharmacokinetics and local neurochemical effects was further investigated.Results: The dynamic profiles of over 10 nicotine metabolites and neurotransmitters were simultaneously obtained after a single injection of nicotine (2 mg·kg−1, i.p.) using the new method. Proadifen pretreatment (50 mg·kg−1·d−1, i.p., 4 days) caused significant inhibition of brain CYP2B1 activity. When exposed to nicotine, the brain Cmax of nicotine was 1.26 times higher and the levels of nicotine metabolites, nornicotine, and nicotine-N-oxide, were decreased by 85.3% and 34.4% in proadifen-pretreated rats. The higher level of brain nicotine induced a greater release of dopamine, serotonin, glutamate, and γ-amino-butyric acid in the nucleus accumbens. The concentrations of nicotine and dopamine were positively correlated, and the average levels of γ-amino-butyric acid and serotonin were 2.7 and 1.2 times higher, respectively, under the inhibition of nicotine metabolism.Discussion: These results demonstrated that inhibiting nicotine metabolism in rats can enhance the residence of brain nicotine and its local neurotransmitter effects. The metabolic activity of nicotine under different physiological conditions could regulate nicotine’s bioavailability and its resulting pharmacology.

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