Effects of propofol and pentobarbital on calcium concentration in presynaptic boutons on a rat hippocampal neuron

S, Itó; Sugiyama, Hitomi; Kitahara, Seiko; Ikemoto, Yoshimi; Yokoyama, Takeshi

doi:10.1007/s00540-011-1186-4

Cited by 8 publications

(9 citation statements)

References 37 publications

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“…In other hand, it is well known that barbituric anesthetics such as thiopental shows GABA A agonist effects on both nerve and synapses [36,37], however, previous report shows evidences that at this level of barbituric anesthesia in rats (absence of nocifencive reflexes but stable blood pressure and cardiopulmonary rhythms) did not changed the discharge pattern and neuronal functional connectivity evaluated by by auto-and cross-correlation in the spinal dorsal horn when compared to unanaesthetized, decerebrated, spinalized rats [18].…”

Section: Discussionmentioning

confidence: 99%

Noxious mechanical heterotopic stimulation induces inhibition of the spinal dorsal horn neuronal network: analysis of spinal somatosensory-evoked potentials

Meléndez-Gallardo

Eblén-Zajjur

2016

Neurol Sci

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Most of the endogenous pain modulation (EPM) involves the spinal dorsal horn (SDH). EPM including diffuse noxious inhibitory controls have been extensively described in oligoneuronal electrophysiological recordings but less attention had been paid to responses of the SDH neuronal population to heterotopic noxious stimulation (HNS). Spinal somatosensory-evoked potentials (SEP) offer the possibility to evaluate the neuronal network behavior, reflecting the incoming afferent volleys along the entry root, SDH interneuron activities and the primary afferent depolarization. SEP from de lumbar cord dorsum were evaluated during mechanical heterotopic noxious stimuli. Sprague-Dawley rats (n = 12) were Laminectomized (T10-L3). The sural nerve of the left hind paw was electrically stimulated (5 mA, 0.5 ms, 0.05 Hz) to induce lumbar SEP. The HNS (mechanic clamp) was applied sequentially to the tail, right hind paw, right forepaw, muzzle and left forepaw during sural stimulation. N wave amplitude decreases (-16.6 %) compared to control conditions when HNS was applied to all areas of stimulation. This effect was more intense for muzzle stimulation (-23.5 %). N wave duration also decreased by -23.6 %. HNS did not change neither the amplitude nor the duration of the P wave but dramatically increases the dispersion of these two parameters. The results of the present study strongly suggest that a HNS applied to different parts of the body is able to reduce the integrated electrical response of the SDH, suggesting that not only wide dynamic range neurons but many others in the SDH are modulated by the EPM.

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Section: Discussionmentioning

confidence: 99%

Noxious mechanical heterotopic stimulation induces inhibition of the spinal dorsal horn neuronal network: analysis of spinal somatosensory-evoked potentials

Meléndez-Gallardo

Eblén-Zajjur

2016

Neurol Sci

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“…influx (Kozinn et al 2006). Previous reports also demonstrated that propofol selectively inhibits calcium entry through the L-type channel in hippocampal neurons and other cells (Sung et al 2005;Ito et al 2011). Considering the role of Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Propofol Protects Against H2O2-Induced Oxidative Injury in Differentiated PC12 Cells via Inhibition of Ca2+-Dependent NADPH Oxidase

et al. 2015

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Propofol (2,6-diisopropylphenol) is a widely used general anesthetic with anti-oxidant activities. This study aims to investigate protective capacity of propofol against hydrogen peroxide (H2O2)-induced oxidative injury in neural cells and whether the anti-oxidative effects of propofol occur through a mechanism involving the modulation of NADPH oxidase (NOX) in a manner of calcium-dependent. The rat differentiated PC12 cell was subjected to H2O2 exposure for 24 h to mimic a neuronal in vitro model of oxidative injury. Our data demonstrated that pretreatment of PC12 cells with propofol significantly reversed the H2O2-induced decrease in cell viability, prevented H2O2-induced morphological changes, and reduced the ratio of apoptotic cells. We further found that propofol attenuated the accumulation of malondialdehyde (biomarker of oxidative stress), counteracted the overexpression of NOX core subunit gp91(phox) (NOX2) as well as the NOX activity following H2O2 exposure in PC12 cells. In addition, blocking of L-type Ca(2+) channels with nimodipine reduced H2O2-induced overexpression of NOX2 and caspase-3 activation in PC12 cells. Moreover, NOX inhibitor apocynin alone or plus propofol neither induces a significant downregulation of NOX activity nor increases cell viability compared with propofol alone in the PC12 cells exposed to H2O2. These results demonstrate that the protective effects of propofol against oxidative injury in PC12 cells are mediated, at least in part, through inhibition of Ca(2+)-dependent NADPH oxidase.

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“…Hippocampal CA1 pyramidal neurons were dissociated from 10 -14 day-old Sprague-Dawley rats as previously described [8]. Briefly, the brain was quickly cut into slices of 400-µm thickness using a microslicer (DTK-3000W; Dosaka EM, Kyoto, Japan).…”

Section: Mechanical Dissociation Of Hippocampal Ca1 Neuronsmentioning

confidence: 99%

“…For disassociation, the slices were placed in a chamber containing standard external solution (500 µl, see description below), and the hippocampal CA1 region was contacted with a fire-polished glass pipette. The pipette was mechanically vibrated horizontally for 1 min using a custom-made device, which caused dissociation of pyramidal neurons along with the attached presynaptic boutons [8] [19].…”

Section: Mechanical Dissociation Of Hippocampal Ca1 Neuronsmentioning

confidence: 99%

“…It is typically thought that propofol mainly affects γ-aminobutyric acid type A (GABA A ) receptors on the postsynaptic membrane of neurons in the central nervous system [1]- [7]. Recently, however, there has been great interest in the effects of propofol on presynaptic events, as several reports have suggested that propofol regulates neurotransmitter release from presynaptic nerve terminals (boutons) [8]- [11]. However, knowledge of the effects of propofol on presynaptic processes remains limited.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Propofol on Glutamate-Induced Calcium Mobilization in Presynaptic Boutons of Rat Hippocampal Neurons

Karube

Sugiyama

et al. 2016

OJAnes

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Recent reports have suggested that various general anesthetics affect presynaptic processes in the central nervous system. However, characterizations of the influence of intravenous anesthetics on neurotransmitter release from presynaptic nerve terminals (boutons) are insufficient. Because the presynaptic calcium concentration ([Ca 2+ ] pre ) regulates neurotransmitter release, we investigate the effects of the intravenous anesthetic propofol on neurotransmitter release by measuring [Ca 2+ ] pre in the presynaptic boutons of individual dissociated hippocampal neurons. Brain slices were prepared from Sprague-Dawley rats (10 -14 days of age). The hippocampal CA1 area was isolated with a fire-polished glass pipette, which vibrated horizontally to dissociate hippocampal CA1 neurons along with their attached presynaptic boutons. Presynaptic boutons were visualized under a confocal laser scanning microscope after staining with FM1-43 dye, and [Ca 2+ ] pre was measured using fluo-3 AM dye. Glutamate (3 -100 µM) administration increased [Ca 2+ ] pre in Ca 2+containing external solution in a concentration-dependent manner. Propofol (3 -30 µM) dosedependently suppressed this glutamate (30 µM)-induced increase in [Ca 2+ ] pre in boutons attached to dendrites, but not to the soma or base of the dendritic tree. The large majority of excitatory synapses on CA1 neurons are located on dendritic spines; therefore, propofol may affect glutamate-induced Ca 2+ mobilization in excitatory, but not inhibitory, presynaptic boutons. Propofol may possibly have some effect on glutamate-regulated neurotransmitter release from excitatory presynaptic nerve terminals through inhibiting the increase in [Ca 2+ ] pre induced by glutamate.

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Effects of propofol and pentobarbital on calcium concentration in presynaptic boutons on a rat hippocampal neuron

Abstract: Propofol and pentobarbital may affect neurotransmitter release from the excitatory presynaptic nerve terminals due to inhibition of increase in [Ca(2+)](pre).

Cited by 8 publications

References 37 publications

Noxious mechanical heterotopic stimulation induces inhibition of the spinal dorsal horn neuronal network: analysis of spinal somatosensory-evoked potentials

Noxious mechanical heterotopic stimulation induces inhibition of the spinal dorsal horn neuronal network: analysis of spinal somatosensory-evoked potentials

Propofol Protects Against H2O2-Induced Oxidative Injury in Differentiated PC12 Cells via Inhibition of Ca2+-Dependent NADPH Oxidase

Effects of Propofol on Glutamate-Induced Calcium Mobilization in Presynaptic Boutons of Rat Hippocampal Neurons

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