Anesthetic-Induced Transitions by Propofol Modeled by Nonlocal Neural Populations Involving Two Neuron Types

Hutt, Axel; Schimansky‐Geier, Lutz

doi:10.1007/s10867-008-9065-4

Cited by 8 publications

(4 citation statements)

References 20 publications

(32 reference statements)

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“…Then a further increase of p causes the stationary excitatory firing activity to discontinuously jump to smaller values. In addition we observe a top, center and bottom solution branch, similar to previous studies (Steyn-Ross et al 2001a;Hutt and Schimansky-Geier 2008). Likewise, the single stationary solution (Fig.…”

Section: The Resting Statesupporting

confidence: 90%

“…The model extends previous standard neural field models of a single cell type by an additional cell population and the action of propofol on the neural field. In addition, it extends a previous model involving two cell types (Hutt and Schimansky-Geier 2008) by the a realistic model for the inhibitory action of anesthetic agents. Moreover, the model is rather simple due to its two field variables and two evolution equations compared to other models such as the Steyn-Ross-model (Steyn-Ross et al 2001a) with 12 field variables and 8 evolution equations.…”

Section: Discussionmentioning

confidence: 74%

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Effects of the anesthetic agent propofol on neural populations

Hutt

Longtin

2009

Cogn Neurodyn

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The neuronal mechanisms of general anesthesia are still poorly understood. Besides several characteristic features of anesthesia observed in experiments, a prominent effect is the bi-phasic change of power in the observed electroencephalogram (EEG), i.e. the initial increase and subsequent decrease of the EEG-power in several frequency bands while increasing the concentration of the anaesthetic agent. The present work aims to derive analytical conditions for this bi-phasic spectral behavior by the study of a neural population model. This model describes mathematically the effective membrane potential and involves excitatory and inhibitory synapses, excitatory and inhibitory cells, nonlocal spatial interactions and a finite axonal conduction speed. The work derives conditions for synaptic time constants based on experimental results and gives conditions on the resting state stability. Further the power spectrum of Local Field Potentials and EEG generated by the neural activity is derived analytically and allow for the detailed study of bi-spectral power changes. We find bi-phasic power changes both in monostable and bistable system regime, affirming the omnipresence of bi-spectral power changes in anesthesia. Further the work gives conditions for the strong increase of power in the d-frequency band for large propofol concentrations as observed in experiments.

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Section: The Resting Statesupporting

confidence: 90%

Section: Discussionmentioning

confidence: 74%

Effects of the anesthetic agent propofol on neural populations

Hutt

Longtin

2009

Cogn Neurodyn

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“…Propofol on its own roughly maintains the α peak frequency with an anteriorization of power (decrease occipital, increase frontal), see Figure 1B; though an additional broadband “beta buzz” just above α frequencies, “biphasic” response dynamics and smooth transitions to lower frequencies can confound the picture (Schwender et al, 1996; Kuizenga et al, 1998, 2001; Feshchenko et al, 2004; Breshears et al, 2010; Cimenser et al, 2011). We assume here from previous theoretical studies (Liley et al, 2003; Hutt and Schimansky-Geier, 2008; Hutt and Longtin, 2010; Hindriks and van Putten, 2012) that these complications can be accounted for by mechanisms not considered in this work, in particular the prominent γ-aminobutyric acid type A (GABA A ) agonism of propofol that affects dominantly inhibitory postsynaptic currents (Kitamura et al, 2003). Furthermore, the acceleration due to ketamine observed by Hayashi et al (2007) and Tsuda et al (2007) that we wish to describe occurred on top of a clear α rhythm at steady propofol concentration, see Figure 1C.…”

Section: Introductionmentioning

confidence: 98%

Ketamine, Propofol, and the EEG: A Neural Field Analysis of HCN1-Mediated Interactions

Bojak¹,

Day²,

Liley³

2013

Front. Comput. Neurosci.

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Ketamine and propofol are two well-known, powerful anesthetic agents, yet at first sight this appears to be their only commonality. Ketamine is a dissociative anesthetic agent, whose main mechanism of action is considered to be N-methyl-d-aspartate (NMDA) antagonism; whereas propofol is a general anesthetic agent, which is assumed to primarily potentiate currents gated by γ-aminobutyric acid type A (GABAA) receptors. However, several experimental observations suggest a closer relationship. First, the effect of ketamine on the electroencephalogram (EEG) is markedly changed in the presence of propofol: on its own ketamine increases θ (4–8 Hz) and decreases α (8–13 Hz) oscillations, whereas ketamine induces a significant shift to beta band frequencies (13–30 Hz) in the presence of propofol. Second, both ketamine and propofol cause inhibition of the inward pacemaker current Ih, by binding to the corresponding hyperpolarization-activated cyclic nucleotide-gated potassium channel 1 (HCN1) subunit. The resulting effect is a hyperpolarization of the neuron’s resting membrane potential. Third, the ability of both ketamine and propofol to induce hypnosis is reduced in HCN1-knockout mice. Here we show that one can theoretically understand the observed spectral changes of the EEG based on HCN1-mediated hyperpolarizations alone, without involving the supposed main mechanisms of action of these drugs through NMDA and GABAA, respectively. On the basis of our successful EEG model we conclude that ketamine and propofol should be antagonistic to each other in their interaction at HCN1 subunits. Such a prediction is in accord with the results of clinical experiment in which it is found that ketamine and propofol interact in an infra-additive manner with respect to the endpoints of hypnosis and immobility.

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“…The simulations of Hutt and SchimanskyGeier [15] are designed for the evaluation of the effects of anaesthetics such as propofol. Their neuronal population model includes excitatory and inhibitory synapses and thereby exhibits a bifurcation structure which can be related to the transitions from consciousness to non-consciousness.…”

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confidence: 99%

Complexity in Neurology and Psychiatry

et al. 2008

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This special issue focuses on the most complex system we know: the brain. More precisely, it deals with the examination of the brain dynamics and disturbances which are clinically manifested in neurological and psychiatric disorders like epilepsy, Parkinson's disease or mental depression. These diseases are often associated with disturbances of autonomous functions like hormone secretion and sleep which also are under the control of the brain. Accordingly, the papers in this issue will refer to a diversity of physiological systems. Their common link is that they all are related to brain functions and dysfunctions and that these neurophysiological issues are addressed by physically based approaches of systems analysis with the use of computer models and tools for nonlinear data analysis.The high expectations in such interdisciplinary approaches towards a better understanding of brain dynamics is the major motivation for this issue. All the authors have expertise in interdisciplinary work and have already made essential contributions in their fields. Many of them are experimental physiologists or clinicians who have learnt to implement biophysical methods, mostly in cooperation with physicists and mathematicians. Vice versa, the physicists and mathematicians among the authors have successfully entered the life sciences in demonstrating that physical applications are not only of interest from a systems theoretical point of view; but can also have high physiological relevance.

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Anesthetic-Induced Transitions by Propofol Modeled by Nonlocal Neural Populations Involving Two Neuron Types

Cited by 8 publications

References 20 publications

Effects of the anesthetic agent propofol on neural populations

Effects of the anesthetic agent propofol on neural populations

Ketamine, Propofol, and the EEG: A Neural Field Analysis of HCN1-Mediated Interactions

Complexity in Neurology and Psychiatry

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