Effects of halothane on GABAergic and glutamatergic transmission in isolated hippocampal nerve-synapse preparations

Kotani, Naoki; Wakita, Masahito; Shin, Min-Chul; Ogawa, Shuji; Nonaka, Kiku; Akaike, Norio

doi:10.1016/j.brainres.2012.07.035

Cited by 10 publications

(5 citation statements)

References 34 publications

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“…Here, it may be important to consider why N 2 O, in contrast to Xe, did not have any effects on the frequency of glutamatergic sEPSCs and GABAergic sIPSCs, despite decreasing the amplitude of both eEPSCs and eIPSCs with the increase of Rf and PPR. Similarly, we have reported marked differences between spontaneous (miniature) and evoked responses in previous anaesthetic studies (Ogawa et al 2011;Kotani et al 2012;Shin et al 2013;Wakita et al 2013Wakita et al , 2015aWakita et al , 2016. The spontaneous and evoked transmitter releases are regulated by different intracellular mechanisms of presynaptic nerve endings.…”

Section: Different Mechanisms Between Spontaneous and Evoked Responsesmentioning

confidence: 51%

“…For eEPSCs and eIPSCs, the amplitude, Rf, PPR and 1/e decay time were also calculated with pCLAMP (Kotani et al 2012). When either the P 1 or the P 2 current failed to appear at the expected latency, the PPR value was not included in the mean PPR data.…”

Section: Discussionmentioning

confidence: 99%

“…These results demonstrate that misunderstandings about mechanisms of anaesthetic actions can arise when one mistakenly extrapolates from whole-cell currents to what may be occurring at the synapse level (Ogawa et al 2011;Kotani et al 2012).…”

Section: Introductionmentioning

confidence: 87%

“…By use of this technique, we have observed how various volatile and intravenous anaesthetics act on glutamatergic excitatory and GABAergic and glycinergic inhibitory postsynaptic currents at the synaptic level and found that synaptic responses to drugs were different from whole-cell responses (Ogawa et al 2011;Kotani et al 2012;Shin et al 2013;Wakita et al 2013Wakita et al , 2015aWakita et al , 2016. For example, four volatile anaesthetics (halothane, enflurane, isoflurane and sevoflurane) enhanced whole-cell currents induced by bath application of GABA (I GABA ), while having no effect or differential effects on miniature inhibitory postsynaptic current (mIPSC) or eIPSC amplitudes and kinetics.…”

Section: Introductionmentioning

confidence: 99%

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Xenon modulates synaptic transmission to rat hippocampal CA3 neurons at both pre‐ and postsynaptic sites

Nonaka

Kotani²,

Akaike

et al. 2019

The Journal of Physiology

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Key points Xenon (Xe) non‐competitively inhibited whole‐cell excitatory glutamatergic current (IGlu) and whole‐cell currents gated by ionotropic glutamate receptors (IAMPA, IKA, INMDA), but had no effect on inhibitory GABAergic whole‐cell current (IGABA). Xe decreased only the frequency of glutamatergic spontaneous and miniature excitatory postsynaptic currents and GABAergic spontaneous inhibitory postsynaptic currents without changing the amplitude or decay times of these synaptic responses. Xe decreased the amplitude of both the action potential‐evoked excitatory and the action potential‐evoked inhibitory postsynaptic currents (eEPSCs and eIPSCs, respectively) via a presynaptic inhibition in transmitter release. We conclude that the main site of action of Xe is presynaptic in both excitatory and inhibitory synapses, and that the Xe inhibition is much greater for eEPSCs than for eIPSCs. Abstract To clarify how xenon (Xe) modulates excitatory and inhibitory whole‐cell and synaptic responses, we conducted an electrophysiological experiment using the ‘synapse bouton preparation’ dissociated mechanically from the rat hippocampal CA3 region. This technique can evaluate pure single‐ or multi‐synapse responses and enabled us to accurately quantify how Xe influences pre‐ and postsynaptic aspects of synaptic transmission. Xe inhibited whole‐cell glutamatergic current (IGlu) and whole‐cell currents gated by the three subtypes of glutamate receptor (IAMPA, IKA and INMDA). Inhibition of these ionotropic currents occurred in a concentration‐dependent, non‐competitive and voltage‐independent manner. Xe markedly depressed the slow steady current component of IAMPA almost without altering the fast phasic IAMPA component non‐desensitized by cyclothiazide. It decreased current frequency without affecting the amplitude and current kinetics of glutamatergic spontaneous excitatory postsynaptic currents and miniature excitatory postsynaptic currents. It decreased the amplitude, increasing the failure rate (Rf) and paired‐pulse rate (PPR) without altering the current kinetics of glutamatergic action potential‐evoked excitatory postsynaptic currents. Thus, Xe has a clear presynaptic effect on excitatory synaptic transmission. Xe did not alter the GABA‐induced whole‐cell current (IGABA). It decreased the frequency of GABAergic spontaneous inhibitory postsynaptic currents without changing the amplitude and current kinetics. It decreased the amplitude and increased the PPR and Rf of the GABAergic action potential‐evoked inhibitory postsynaptic currents without altering the current kinetics. Thus, Xe acts exclusively at presynaptic sites at the GABAergic synapse. In conclusion, our data indicate that a presynaptic decrease of excitatory transmission is likely to be the major mechanism by which Xe induces anaesthesia, with little contribution of effects on GABAergic synapses.

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Section: Different Mechanisms Between Spontaneous and Evoked Responsesmentioning

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Xenon modulates synaptic transmission to rat hippocampal CA3 neurons at both pre‐ and postsynaptic sites

Nonaka

Kotani²,

Akaike

et al. 2019

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Fortunately, we developed the "synaptic bouton" preparation, which allows the pharmacological effects of various drugs on the excitatory and inhibitory neurotransmissions at the single synapse level to be observed using mechanically dissociated mammalian central nervous system (CNS) neurons (Akaike and Moorhouse, 2003;Kotani et al, 2012;Shin et al, 2013;Wakita et al, 2012). Thus, the "synaptic bouton" preparation limits the effects of confounding factors on the indirect sites of Li + action, such as adjacent neurons and glial cells surrounding the target hippocampal neurons.…”

Section: Introductionmentioning

confidence: 99%

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment

Wakita¹,

Nagami²,

Takase³

et al. 2015

Brain Research Bulletin

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Effects of Etomidate on GABAergic and Glutamatergic Transmission in Rat Thalamocortical Slices

Wang

Yang

et al. 2016

Neurochem Res

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Although accumulative evidence indicates that the thalamocortical system is an important target for general anesthetics, the underlying mechanisms of anesthetic action on thalamocortical neurotransmission are not fully understood. The aim of the study is to explore the action of etomidate on glutamatergic and GABAergic transmission in rat thalamocortical slices by using whole cell patch-clamp recording. We found that etomidate mainly prolonged the decay time of spontaneous GABAergic inhibitory postsynaptic currents (sIPSCs), without changing the frequency. Furthermore, etomidate not only prolonged the decay time of miniature inhibitory postsynaptic currents (mIPSCs) but also increased the amplitude. On the other hand, etomidate significantly decreased the frequency of spontaneous glutamatergic excitatory postsynaptic currents (sEPSCs), without altering the amplitude or decay time in the absence of bicuculline. When GABA receptors were blocked using bicuculline, the effects of etomidate on sEPSCs were mostly eliminated. These results suggest that etomidate enhances GABAergic transmission mainly through postsynaptic mechanism in thalamocortical neuronal network. Etomidate attenuates glutamatergic transmission predominantly through presynaptic action and requires presynaptic GABA receptors involvement.

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Effects of halothane on GABAergic and glutamatergic transmission in isolated hippocampal nerve-synapse preparations

Cited by 10 publications

References 34 publications

Xenon modulates synaptic transmission to rat hippocampal CA3 neurons at both pre‐ and postsynaptic sites

Xenon modulates synaptic transmission to rat hippocampal CA3 neurons at both pre‐ and postsynaptic sites

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment

Effects of Etomidate on GABAergic and Glutamatergic Transmission in Rat Thalamocortical Slices

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