Neonatal Exposure to Sevoflurane Causes Significant Suppression of Hippocampal Long-Term Potentiation in Postgrowth Rats

Kato, Rumiko; Tachibana, Kaori; Nishimoto, Norihiro; Hashimoto, Toshikazu; Uchida, Yoshiyuki; Ito, Ryoko; Tsuruga, Kenkichi; Takita, Kensuke; Morimoto, Yuji

doi:10.1213/ane.0b013e3182a8c709

Cited by 39 publications

(25 citation statements)

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“…Second, the effect of propofol on synaptic function was not studied. In addition to synaptic density, synaptic plasticity and synaptic neurotransmissions play an important role in learning and memory as well (Jevtovic-Todorovic et al, 2003;Kato et al, 2013;Sanchez et al, 2011). Further studies are needed to determine whether propofol of different exposure times can affect synaptic function at different time points with brain development.…”

Section: Discussionmentioning

confidence: 99%

Persistent neuronal apoptosis and synaptic loss induced by multiple but not single exposure of propofol contribute to long-term cognitive dysfunction in neonatal rats

et al. 2016

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-Propofol can induce acute neuronal apoptosis or long-term cognitive dysfunction when exposed at early age in rodents, but it is unclear how the neurotoxicity including neuronal apoptosis and synaptic loss will change in a dynamic manner with brain development after multiple or single exposure of propofol, and the role of neuronal apoptosis and synaptic loss in propofol-induced long-term cognitive impairment needs to be elucidated. In this study, we investigated dynamic changes of neuronal apoptosis, neuronal density, synaptic density in hippocampal CA1 region and the prelimbic cortex (PrL), and longterm cognitive function after multiple or single exposure of propofol in neonatal rats. Results showed that single exposure of propofol only induced great neuronal apoptosis and deficit at postnatal day 9(P9); while multiple exposures of propofol could induce significant neuronal apoptosis, neuronal deficit and synaptic loss at P9, P14, P21, or P35 compared with intact, and spatial learning and memory impairment from P36 to P41. Results suggest that single exposure of propofol only induces transient neuronal apoptosis and deficit, while multiple exposures of propofol induce persistent neuronal apoptosis, neuronal deficit, synaptic loss, and long-term cognitive impairment. Furthermore, persistent neuronal deficit and disturbances in synapse formation but not transient neuronal apoptosis may contribute to long-term cognitive impairment.

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Section: Discussionmentioning

confidence: 99%

Persistent neuronal apoptosis and synaptic loss induced by multiple but not single exposure of propofol contribute to long-term cognitive dysfunction in neonatal rats

et al. 2016

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“…mEPSCs are evoked by single vesicle release, which is triggered by release of presynaptic calcium ions (35). Alterations to the frequency and amplitude of mEPSCs are ascribed to presynaptic and postsynaptic action (36). The amplitude of mEPSCs reflects the response of the postsynaptic receptor to a single vesicle, while the frequency is partially due to changes to the presynaptic calcium channel (35).…”

Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane on leucine-rich repeat kinaseï¿½2-associated Drosophila model of Parkinson's disease

et al. 2014

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Abstract.Patients with Parkinson's disease (PD) often require surgery, and therefore may receive inhalation anesthesia. However, it is currently unknown whether inhalation anesthetics affect the prognosis of the disease. Leucine-rich repeat kinase 2 (LRRK2) genetic mutations are the most common cause of familial PD, contributing to ~39% of all cases in certain populations. The aim of the present study was to determine the effects of inhaled anesthetics on PD, by observing the influence of sevoflurane on a LRRK2-associated Drosophila model of PD. PD transgenic Drosophila overexpressing LRRK2 were generated by crossing flies expressing an LRRK2 upstream activation sequence, with tyrosine hydroxylase (TH)-Gal4 flies. Western blot analysis successfully verified that the transgenic Drosophila overexpressed LRRK2. Three days prior to eclosion, three genotypes of Drosophila were divided into four groups, and were exposed to air, 1, 2, or 3% sevoflurane, for 5 hours. Twenty-four hours after the exposure, the electrophysiological activities of the projection neurons (PN) in the brains of the Drosophila were recorded using a patch clamp. The locomotor activities were tested on days 5,10,15,20, 25,30,35 and 40 following eclosion. The frequency of miniature excitatory synaptic currents (mEPSCs) obtained from the PNs of the TH-wild type LRRK2 (TH-WT) Drosophila brain, following exposure to air (1.60±0.05 Hz), was lower as compared with the wild type LRRK2 (WT) (2.51±0.07 Hz) and W1118 (2.41±0.10 Hz) Drosophila. After exposure to 1, 2 and 3% sevoflurane, the frequency of mEPSCs in the brains of the TH-WT group decreased to 0.82±0.04 Hz, 0.63±0.16 Hz and 0.55±0.04 Hz, respectively. The percentage decrease of the frequency of mEPSCs, from exposure to air to 1% sevoflurane, of the TH-WT group (48.32%±3.08%) was significantly higher, as compared with the WT (39.17%±1.42%) and W1118 (35.10%±2.66%) groups, and there was no statistical difference between the WT and W1118 groups. The transgenic TH-WT Drosophila presented an early decrease in locomotor ability, as compared with the WT and W1118 groups. Following a 5 hour exposure to sevoflurane, the percentage decrease of the climbing abilities of the TH-WT group, from exposure to air to 1% sevoflurane, were significantly lower, as compared with the WT and W1118 groups. In conclusion, sevoflurane had negative effects on the control W1118 flies, and also severely aggravated the prognosis of PD in the LRRK2-associated Drosophila model, through synaptic cholinergic deficits and impairment on locomotor abilities.

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“…Evidence is conclusive in developing models of in vitro and in vivo rodent brain that isoflurane provides a duration- and dose-dependent effect on neuronal cell death [5,18,22]. Studies have looked at sevoflurane, independently and in comparison to isoflurane, and have found neuronal cell death as well [6,8,19,20,21,66,68,70]. Long-term outcome appears to be potentially similar with both agents but early or short-term memory may not be impaired with sevoflurane [21].…”

Section: The Choice Of Anestheticmentioning

confidence: 99%

“…Indeed, clinical anesthetic care in these children has improved and the practice of providing anesthesia has changed, numerous anesthetics have been performed in young infants and children without obvious neurologic complications. However, beyond the clinical science, basic science may offer a different perspective [5,6,7,8]. …”

Section: Introductionmentioning

confidence: 99%

“…These neurologic outcome studies are specific to the preterm [9,10,11] and congenital heart disease populations [12,13,14,15,16,17]. With the recent concern of anesthetic neurotoxicity in the developing brain, mostly from laboratory investigations [5,6,7,8,18,19,20,21,22] the neurologic assessment of children after anesthetic exposure at a young age is now being emphasized [23,24,25,26,27,28,29,30]. …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Anesthesia and the Developing Brain: Relevance to the Pediatric Cardiac Surgery

2014

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Anesthetic neurotoxicity has been a hot topic in anesthesia for the past decade. It is of special interest to pediatric anesthesiologists. A subgroup of children potentially at greater risk for anesthetic neurotoxicity, based on a prolonged anesthetic exposure early in development, are those children receiving anesthesia for surgical repair of congenital heart disease. These children have a known risk of neurologic deficit after cardiopulmonary bypass for surgical repair of congenital heart disease. Yet, the type of anesthesia used has not been considered as a potential etiology for their neurologic deficits. These children not only receive prolonged anesthetic exposure during surgical repair, but also receive repeated anesthetic exposures during a critical period of brain development. Their propensity to abnormal brain development, as a result of congenital heart disease, may modify their risk of anesthetic neurotoxicity. This review article provides an overview of anesthetic neurotoxicity from the perspective of a pediatric cardiac anesthesiologist and provides insight into basic science and clinical investigations as it relates to this unique group of children who have been studied over several decades for their risk of neurologic injury.

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Neonatal Exposure to Sevoflurane Causes Significant Suppression of Hippocampal Long-Term Potentiation in Postgrowth Rats

Abstract: Our present findings indicate that neonatal exposure to sevoflurane at a higher concentration can cause alterations in the hippocampal synaptic plasticity that persists into adulthood.

Cited by 39 publications

References 37 publications

Persistent neuronal apoptosis and synaptic loss induced by multiple but not single exposure of propofol contribute to long-term cognitive dysfunction in neonatal rats

Persistent neuronal apoptosis and synaptic loss induced by multiple but not single exposure of propofol contribute to long-term cognitive dysfunction in neonatal rats

Effects of sevoflurane on leucine-rich repeat kinaseï¿½2-associated Drosophila model of Parkinson's disease

Anesthesia and the Developing Brain: Relevance to the Pediatric Cardiac Surgery

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