Disruption of muscarinic receptor-G protein coupling is a general property of liquid volatile anesthetics

Anthony, Betty L.; Dennison, Robert L.; Aronstam, Robert S.

doi:10.1016/0304-3940(89)90288-7

Cited by 49 publications

(14 citation statements)

References 9 publications

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“…We decided to perform these experiments in the anesthetized animal, because this preparation allows investigating more stimulus conditions with and without drug applied than is feasible in the awake animal, especially in animals performing attention-demanding tasks. However, anesthesia interacts with the cholinergic and GABAergic systems (Anthony et al, 1989;Yamakura et al, 2001;Tassonyi et al, 2002), which may have implications for our results, especially regarding our findings in relation to noise correlations and FFs. If halothane induced a synchronized brain state (Harris and Thiele, 2011), then noise correlations might be increased overall, and alterations seen with, for example, ACh might be much larger than what would occur in awake animals.…”

Section: Interaction With Anesthesiamentioning

confidence: 54%

Contribution of Cholinergic and GABAergic Mechanisms to Direction Tuning, Discriminability, Response Reliability, and Neuronal Rate Correlations in Macaque Middle Temporal Area

et al. 2012

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Previous studies have investigated the effects of acetylcholine (ACh) on neuronal tuning, coding, and attention in primary visual cortex, but its contribution to coding in extrastriate cortex is unexplored. Here we investigate the effects of ACh on tuning properties of macaque middle temporal area MT neurons and contrast them with effects of gabazine, a GABA A receptor blocker. ACh increased neuronal activity, it had no effect on tuning width, but it significantly increased the direction discriminability of a neuron. Gabazine equally increased neuronal activity, but it widened tuning curves and decreased the direction discriminability of a neuron. Although gabazine significantly reduced response reliability, ACh application had little effect on response reliability. Finally, gabazine increased noise correlation of simultaneously recorded neurons, whereas ACh reduced it. Thus, both drugs increased firing rates, but only ACh application improved neuronal tuning and coding in line with effects seen in studies in which attention was selectively manipulated.

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Section: Interaction With Anesthesiamentioning

confidence: 54%

Contribution of Cholinergic and GABAergic Mechanisms to Direction Tuning, Discriminability, Response Reliability, and Neuronal Rate Correlations in Macaque Middle Temporal Area

et al. 2012

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“…Inhaled anesthetics affect protein-protein interaction by disrupting heteromeric [1] and homomeric [2] binding in some cases and by promoting such interactions in others [3, 4]. These observations warrant further examination of the interfacial cavities that regulate protein-protein interaction.…”

Section: Introductionmentioning

confidence: 99%

Inhaled Anesthetics Promote Albumin Dimerization through Reciprocal Exchange of Subdomains

Pieters

Fibuch

Eklund

et al. 2010

Biochemistry Research International

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Inhaled anesthetics affect protein-protein interaction, but the mechanisms underlying these effects are still poorly understood. We examined the impact of sevoflurane and isoflurane on the dimerization of human serum albumin (HSA), a protein with anesthetic binding sites that are well characterized. Intrinsic fluorescence emission was analyzed for spectral shifting and self-quenching, and control first derivatives (spectral responses to changes in HSA concentration) were compared against those obtained from samples treated with sevoflurane or isoflurane. Sevoflurane increased dimer-dependent self-quenching and both decreased oligomer-dependent spectral shifting, suggesting that inhaled anesthetics promoted HSA dimerization. Size exclusion chromatography and polarization data were consistent with these observations. The data support the proposed model of a reciprocal exchange of subdomains to form an HSA dimer. The open-ended exchange of subdomains, which we propose occuring in HSA oligomers, was inhibited by sevoflurane and isoflurane.

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“…Several groups have indeed shown that volatile anesthetics may interfere with this finely balanced signal transduction cascade. Chloroform, enflurane, isoflurane, and halothane increased binding affinity of 3 H-methylscopolamine to muscarinic receptors, but not that of agonists, and eliminated the guanine nucleotide shift of high-affinity agonist binding suggesting disruption of muscarinic receptor-G protein coupling by volatile anesthetics (Anthony et al, 1989). These results were confirmed by another study demonstrating an increased binding affinity of 3 H-quinuclidinylbenzilate to muscarinic receptors in the presence of halothane, however, with a reduced number of binding sites, whereas binding of 125 I-iodocyanopindolol to β-adrenoceptors remained unaltered (Böhm et al, 1993).…”

Section: Interaction Of Volatile Anesthetics (And Halocarbons) With Cmentioning

confidence: 95%

Mechanisms Involved in Cardiac Sensitization by Volatile Anesthetics: General Applicability to Halogenated Hydrocarbons?

Himmel

2008

Critical Reviews in Toxicology

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An increased sensitivity of the heart to catecholamines or cardiac sensitization is a recognized risk during acute human exposure to halogenated hydrocarbons used as solvents, foam-blowing or fire-extinguishing agents, refrigerants, and aerosol propellants. Although cardiac sensitization to such "industrial" halocarbons can result in serious arrhythmia and death, research into its mechanistic basis has been limited, whereas the literature on volatile anesthetics (e.g., halothane, chloroform) is comparably extensive. A review of the literature on halocarbons and related volatile anesthetics was conducted. The available experimental evidence suggests that volatile anesthetics at physiologically relevant concentrations interact predominantly with the main repolarizing cardiac potassium channels hERG and I Ks , as well as with calcium and sodium channels at slightly higher concentrations. On the level of the heart, inhibition of these ion channels is prone to alter both action potential shape (triangulation) and electrical impulse conduction, which may facilitate arrhythmogenesis by volatile anesthetics per se and is potentiated by catecholamines. Action potential triangulation by regionally heterogeneous inhibition of calcium and potassium channels will facilitate catecholamine-induced afterdepolarizations, triggered activity, and enhanced automaticity. Inhibition of cardiac sodium channels will reduce conduction velocity and alter refractory period; this is potentiated by catecholamines and promotes reentry arrhythmias. Other cardiac and/or neuronal mechanisms might also contribute to arrhythmogenesis. The few scattered in vitro data available for halocarbons (e.g., FC-12, halon 1301, trichloroethylene) suggest inhibition of cardiac sodium (conduction), calcium and potassium channels (triangulation), extraneuronal catecholamine reuptake, and various neuronal ion channels. Therefore, it is hypothesized that halocarbons promote cardiac sensitization by similar mechanisms as volatile anesthetics. Experimental approaches for further investigation of these sensitization mechanisms by selected halocarbons are suggested.

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Disruption of muscarinic receptor-G protein coupling is a general property of liquid volatile anesthetics

Cited by 49 publications

References 9 publications

Contribution of Cholinergic and GABAergic Mechanisms to Direction Tuning, Discriminability, Response Reliability, and Neuronal Rate Correlations in Macaque Middle Temporal Area

Contribution of Cholinergic and GABAergic Mechanisms to Direction Tuning, Discriminability, Response Reliability, and Neuronal Rate Correlations in Macaque Middle Temporal Area

Inhaled Anesthetics Promote Albumin Dimerization through Reciprocal Exchange of Subdomains

Mechanisms Involved in Cardiac Sensitization by Volatile Anesthetics: General Applicability to Halogenated Hydrocarbons?

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