Propofol enhances facial stimulation-evoked responses in the cerebellar granule cell layer via NMDA receptor activation in mice in vivo

Jin, Wen-Zhe; Liu, Heng; Wan, Peng; Chu, Chun-Ping; Qiu, De-Lai

doi:10.1016/j.ejphar.2016.05.027

Cited by 7 publications

(6 citation statements)

References 34 publications

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“…Propofol attenuated the neurotoxic effect of glutamate exerted via activation of NMDA receptors in cultured hippocampal neurons, while augmented the NMDA-mediated effect on intracellular calcium in a cerebral ischemia model (Zhan et al, 2001). Blockade of NMDA receptor activity not only inhibited facial stimulation-evoked responses in mouse cerebellar granule cell layer, but also abolished their enhancement by propofol, suggesting that propofol enhanced granule cell layer responses via modulation of NMDA receptor (Jin et al, 2016). In addition, intravenous administration of propofol depressed the activity of nigral DA neurons, which was prevented by the selective GABA B -receptor antagonist, suggesting that activation of central GABA B receptors may contribute to the anesthetic properties of propofol (Schwieler et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Propofol Inhibits Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission via Activation of Presynaptic GABAB Receptors in vitro in Mice

et al. 2018

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Propofol is a widely used intravenous sedative-hypnotic agent, which causes rapid and reliable loss of consciousness via activation of γ -aminobutyric acid A (GABAA) receptors. We previously found that propofol inhibited cerebellar Purkinje cells (PC) activity via both GABAA and glycine receptors in vivo in mice. We here examined the effect of propofol on the cerebellar parallel fiber (PF)-PC synaptic transmission in mouse cerebellar slices by whole-cell recording technique and pharmacological methods. We found that following blockade of GABAA and glycine receptors activity, propofol reversely decreased the amplitude of PF-PC excitatory postsynaptic currents (PF-PC EPSCs), and significantly increased paired-pulse ratio (PPR). The propofol-induced decrease in amplitude of PF-PC EPSCs was concentration-dependent. The half-inhibitory concentration (IC50) of propofol for inhibiting PF-PC EPSCs was 4.7 μM. Notably, the propofol-induced changes in amplitude and PPR of PF-PC EPSCs were abolished by GABAB receptor antagonist, saclofen (10 μM), but not blocked by N-methyl-D-aspartate receptor (NMDA) receptor antagonist, D-APV (50 μM). Application of the GABAB receptor agonist baclofen induced a decrease in amplitude and an increase in PPR of PF-PC EPSCs, as well masked the propofol-induced changes in PF-PC EPSCs. Moreover, the propofol-induced changes in amplitude and PPR of PF-PC EPSCs were abolished by a specific protein kinase A (PKA) inhibitor, KT5720. These results indicate that application of propofol facilitates presynaptic GABAB receptors, resulting in a depression of PF-PC synaptic transmission via PKA signaling pathway in mouse cerebellar cortex. The results suggest that the interaction with GABAB receptors may contribute to the general anesthetic action of propofol.

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Section: Introductionmentioning

confidence: 99%

Propofol Inhibits Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission via Activation of Presynaptic GABAB Receptors in vitro in Mice

et al. 2018

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“…In cerebellar cortex, NMDA receptors are found on the membrane of GCs and their axonal boutons, which play critical roles in modulation of MF-GC synaptic transmission and plasticity in cerebellar cortex [30][31][32][34][35][36][37] . Notably, our results showed that blocking NMDA receptor depressed the MF-GC synaptic transmission, and abolished the enhancement of the facial stimulation-evoked MF-GC synaptic transmission in the VPA-induced ASD mice.…”

Section: Discussionmentioning

confidence: 99%

“…NMDARs are found on the membrane of cerebellar granule cells (GCs) and parallel ber boutons, which play critical roles in sensory information processing, synaptic plasticity, motor learning and memory, neuropathy and disorder of cerebellum [30][31][32] . The expression of GluN2A and GluN2C mRNA were demonstrated in cerebellar GCs during the second postnatal week, whereas the expression of GluN2B mRNA was transiently expressed in GCs during the rst two postnatal weeks in rats 33 .…”

Section: Introductionmentioning

confidence: 99%

Gestational VPA exposure enhances facial stimulation-evoked cerebellar mossy fiber–granule cell transmission via GluN2A-contanning NMDA receptor in offspring mice

Qiu,

Yuan,

Liu

et al. 2024

Preprint

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Valproic acid (VPA) is one of the most efficient antiepileptic drugs, which exposed during gestation has been employed as an animal model for autism spectrum disorder (ASD). Numerous studies have demonstrated that the dysfunction of synaptic transmission of cerebellar cortical circuitry contributes to the social deficits and repetitive behaviors of ASD. In this study, we investigated the effect of VPA exposure during pregnancy on the tactile stimulation-evoked cerebellar mossy fibers-granule cell (MF-GC) synaptic transmission in the urethane-anesthetized mice. Three-chamber test showed that VPA-exposed mice exhibited significant reduction of social interaction comparted with control group. In vivo electrophysiological recordings revealed that a paired-facial stimulation evoked MF-GC synaptic, N1 and N2. The evoked MF-GC synaptic responses in VPA-exposed mice exhibited a significant increase in area under the curve (AUC) of N1, amplitude and AUC of N2 than that of VPA-untreated mice. Cerebellar surface application of a selective N-methyl-D-aspartate (NMDA) receptors blocker, D-APV, significantly depressed the facial stimulation-evoked MF-GC synaptic transmission. In presence of D-APV, AUC of N1, amplitude and AUC of N2 in VPA-exposed mice were no significant than that of VPA-untreated mice. Notably, blockade of GluN2A- but not GluN2B- subunit-containing NMDA receptor, significantly depressed the MF-GC synaptic transmission, and decreased AUC of N1, amplitude and AUC of N2 in VPA-exposed mice to a similar level of that in VPA-untreated mice. In addition, the expression of GluN2A subunit-containing NMDA receptor immunoreactivity in granule cell layer of VPA-treated mice was significantly higher than that in control mice. These results indicate gestational VPA exposure produces behaviors of ASD accompanied with an enhancement of the cerebellar MF-GC synaptic transmission by an increase of GluN2A-contanning NMDA receptor in offspring mice.

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“…N-methyl-D-aspartate receptor (NMDAR), a subset of ionic glutamic acid receptor which is controlled by the membrane potential as well as by other neurotransmitters, plays an important role in the synaptic transmission and plasticity regulation in the central nervous system ( 44 ). By inhibiting glutamic acid release in the presynaptic element, propofol with clinical concentration induces the allosteric regulation of various sub-units of NMDAR, conducts negative controls, and produces sedative effects ( 45 ).…”

Section: Influence and Acting Sites Of Intravenous Anesthetics On Tumorsmentioning

confidence: 99%

Systemic immune effects of anesthetics and their intracellular targets in tumors

Luan

Sun

et al. 2022

Front. Med.

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According to the result released by the World Health Organization (WHO), non-communicable diseases have occupied four of the top 10 current causes for death in the world. Cancer is one of the significant factors that trigger complications and deaths; more than 80% cancer patients require surgical or palliative treatment. In this case, anesthetic treatment is indispensable. Since cancer is a heterogeneous disease, various types of interventions can activate oncogenes or mutate tumor suppressor genes. More and more researchers believe that anesthetics have a certain effect on the long-term recurrence and metastasis of tumors, but it is still controversial whether they promote or inhibit the progression of cancer. On this basis, a series of retrospective or prospective randomized clinical trials have been conducted, but it seems to be difficult to reach a conclusion within 5 years or longer. This article focuses on the effects of anesthetic drugs on immune function and cancer and reviews their latest targets on the tumor cells, in order to provide a theoretical basis for optimizing the selection of anesthetic drugs, exploring therapeutic targets, and improving the prognosis of cancer patients.

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Propofol enhances facial stimulation-evoked responses in the cerebellar granule cell layer via NMDA receptor activation in mice in vivo

Cited by 7 publications

References 34 publications

Propofol Inhibits Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission via Activation of Presynaptic GABAB Receptors in vitro in Mice

Propofol Inhibits Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission via Activation of Presynaptic GABAB Receptors in vitro in Mice

Gestational VPA exposure enhances facial stimulation-evoked cerebellar mossy fiber–granule cell transmission via GluN2A-contanning NMDA receptor in offspring mice

Systemic immune effects of anesthetics and their intracellular targets in tumors

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