Detrimental effects of postnatal exposure to propofol on memory and hippocampal LTP in mice

Wang, Yuan-Lin; Chen, Xin; Wang, Zhiping

doi:10.1016/j.brainres.2015.06.044

Cited by 11 publications

(5 citation statements)

References 24 publications

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“…Some studies have suggested that toxins, such as propofol and arsenic, could impair basal synaptic transmission, hippocampal LTP, and memory, along with decreased p-Akt levels. 32,33 Our results showed that p-Akt was significantly downregulated in 3.5 nm MPA-modified CdTe QD exposure, which indicated that dysfunction of the PI3K-Akt signaling pathway might be one of the mechanisms of CNS impairment induced by MPA-modified CdTe QD exposure. However, the effects of 3.5 nm MPA-modified CdTe QDs on the phosphorylation of Akt are complicated in view of the findings that the mRNA level of the gene PIK3R5 (encoding PI3K) was significantly upregulated in high-dose 3.5 nm MPA-modified CdTe QD exposure, and decreased p-Akt levels were not dose-dependent.…”

mentioning

confidence: 66%

Impairments of spatial learning and memory following intrahippocampal injection in rats of 3-mercaptopropionic acid-modified CdTe quantum dots and molecular mechanisms

Wu¹,

He²,

Ang³

et al. 2016

IJN

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With the rapid development of nanotechnology, quantum dots (QDs) as advanced nanotechnology products have been widely used in neuroscience, including basic neurological studies and diagnosis or therapy for neurological disorders, due to their superior optical properties. In recent years, there has been intense concern regarding the toxicity of QDs, with a growing number of studies. However, knowledge of neurotoxic consequences of QDs applied in living organisms is lagging behind their development, even if several studies have attempted to evaluate the toxicity of QDs on neural cells. The aim of this study was to evaluate the adverse effects of intrahippocampal injection in rats of 3-mercaptopropionic acid (MPA)-modified CdTe QDs and underlying mechanisms. First of all, we observed impairments in learning efficiency and spatial memory in the MPA-modified CdTe QD-treated rats by using open-field and Y-maze tests, which could be attributed to pathological changes and disruption of ultrastructure of neurons and synapses in the hippocampus. In order to find the mechanisms causing these effects, transcriptome sequencing (RNA-seq), an advanced technology, was used to gain the potentially molecular targets of MPA-modified CdTe QDs. According to ample data from RNA-seq, we chose the signaling pathways of PI3K–Akt and MPAK–ERK to do a thorough investigation, because they play important roles in synaptic plasticity, long-term potentiation, and spatial memory. The data demonstrated that phosphorylated Akt (p-Akt), p-ERK1/2, and c-FOS signal transductions in the hippocampus of rats were involved in the mechanism underlying spatial learning and memory impairments caused by 3.5 nm MPA-modified CdTe QDs.

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mentioning

confidence: 66%

Impairments of spatial learning and memory following intrahippocampal injection in rats of 3-mercaptopropionic acid-modified CdTe quantum dots and molecular mechanisms

Wu¹,

He²,

Ang³

et al. 2016

IJN

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“…General anesthetics, not only affect the development of neurons, but also damage them ( 4 , 5 ). Previous findings have demonstrated that general anesthetics cause extensive cell death in the brain, reduce the number of brain cells and decrease synaptic function, resulting in cognitive impairment, and this damage extends to adulthood ( 20 , 21 ). Neonatal rats are the most commonly used model to investigate neurodevelopment ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

“…Neuronal apoptosis is an important component of neurotoxicity ( 28 , 29 ). In immature animal neurons, general anesthesia produces severe cytotoxicity, particularly in synaptic growth ( 20 , 21 ). In the present study, two different methods were utilized to detect apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of compound 21, a non‑peptide angiotensin II type 2 receptor agonist, on general anesthesia‑induced cerebral injury in neonatal rats

Yong

Wang

et al. 2018

Mol Med Report

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General anesthesia has a great impact on neurodevelopment. However, the mechanisms underlying this effect and therapeutic methods to address it remain limited. The present study aimed to investigate the effects of compound (C)21, a non-peptide angiotensin II type 2 receptor agonist, on general anesthesia-induced cerebral injury in neonatal rats. Neonatal Sprague Dawley rats (postnatal day 7) were randomly divided into three groups (n=6 per group): The control, isoflurane and C21+ isoflurane (C21) group. General anesthesia was induced through inhalation of 1.3% isoflurane. Apoptosis and synaptic structure were analyzed. The levels of peroxisome proliferator-activated receptor (PPAR)-α were detected using an enzyme-linked immunosorbent assay. BCL2, apoptosis regulator (Bcl-2) expression was also measured. Compared with the control group, the cerebral cortex, hippocampus, amygdala and hypothalamus in the isoflurane group had significantly more apoptotic cells (P<0.05). The nuclei of the control group were round and transparent, while shrunken nuclei and condensed chromatin were visible in the isoflurane group. A reduction in synapse number was observed in the isoflurane group compared with the control. By contrast, nuclei shrinkage and the decrease in synaptic number was improved in the C21 group. PPAR-α and Bcl-2 expression, at the mRNA and protein levels, was significantly reduced in the isoflurane group compared with the control (P<0.05). C21 treatment reduced the decrease in PPAR-α and Bcl-2 in the cerebral cortex, hippocampus, amygdala and hypothalamus (P<0.05). Collectively, it was demonstrated that C21 prevented apoptosis and synaptic loss induced by general anesthesia in neonatal rats by enhancing the expression of PPAR-α and Bcl-2.

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“…Another component of synaptic plasticity is long‐term enhancement of synaptic response after transient high‐frequency stimulation. Early birth exposure to the intravenous anaesthetic propofol and volatile anaesthetic sevoflurane has been reported to impair LTP in the adult hippocampus 53,54 . More and more reports have pointed out that sexual neurosteroids play an important role in memory formation, among which estrogen and androgens are more influential in learning and memory 55 cognitive motor adaptation to emotional behaviour development, 56 they regulate synaptic formation LTP and long‐term depression (LTD) of dendritic spinogenesis and synaptic transmission function play an important role in the nervous system development throughout the life cycle.…”

Section: The Role Of Neuroactive Steroids In Sex Differences In Devel...mentioning

confidence: 99%

“…Early birth exposure to the intravenous anaesthetic propofol and volatile anaesthetic sevoflurane has been reported to impair LTP in the adult hippocampus. 53,54 More and more reports have pointed out that sexual neurosteroids play an important role in memory formation, among which estrogen and androgens are more influential in learning and memory 55 cognitive motor adaptation to emotional behaviour development, 56 they regulate synaptic formation LTP and long-term depression (LTD) of den-dritic spinogenesis and synaptic transmission function play an important role in the nervous system development throughout the life cycle. These neurosteroids are synthesized by specific enzymes in the central nervous system to convert cholesterol to pregnenolone to produce testosterone, which is then metabolized to form 5α -dihydrotestosterone (DHT) or 17β -E2 through the action of 5α-reductase or P450 aromatase, respectively.…”

Section: Synaptic Plasticitymentioning

confidence: 99%

The effect of neuroactive steroids in sex differences in the developmental neurotoxicity of the anaesthetic

Zhu

Zeng

et al. 2022

Clinical and Translational Dis

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The rapid growth of the number of surgical cases in the world has brought opportunities and challenges to the development of anaesthesia. Modern anaesthesia technology provides safe and effective anaesthesia for hundreds of millions of surgical procedures each year, but there is a lot of concern about the complications (mainly cognitive dysfunction) that occur after anaesthesia exposure. Preclinical studies have demonstrated cognitive dysfunction and behavioural abnormalities that persist into adulthood after exposure to anaesthesia in rodents, revealing the potential neurotoxicity of anaesthetic drugs. In a further study, Sprague-Dawley rats treated with sevoflurane in the first week of life were then subjected to behavioural tests, and female rats were significantly more negatively affected in spatial learning than male rats, suggesting that there may be gender differences in neurotoxicity of the anaesthetic, but the specific mechanisms are unclear. According to the available data, the main hypothesis that can explain the sex difference in the effect of anaesthesia on the central nervous system development remains the difference in hormone levels between males and females. Therefore, this review briefly describes the role of neuroactive steroids in the mechanism of sex differences in neurotoxicity during the development of general anaesthetics.

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Detrimental effects of postnatal exposure to propofol on memory and hippocampal LTP in mice

Cited by 11 publications

References 24 publications

Impairments of spatial learning and memory following intrahippocampal injection in rats of 3-mercaptopropionic acid-modified CdTe quantum dots and molecular mechanisms

Impairments of spatial learning and memory following intrahippocampal injection in rats of 3-mercaptopropionic acid-modified CdTe quantum dots and molecular mechanisms

Effects of compound 21, a non‑peptide angiotensin II type 2 receptor agonist, on general anesthesia‑induced cerebral injury in neonatal rats

The effect of neuroactive steroids in sex differences in the developmental neurotoxicity of the anaesthetic

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