Emergent Bursting in Small Networks of Model Conditional Pacemakers in the pre-Bötzinger Complex

Rubin, Jonathan E.

doi:10.1007/978-0-387-73693-8_21

Cited by 3 publications

(2 citation statements)

References 7 publications

(16 reference statements)

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“…This raises an important question: what is the significance of intrinsic bursting properties for the generation of the breathing rhythm? Theoretical studies have shown that the presence of intrinsic bursters is not required to generate network-wide bursting (Rubin 2006, 2008), but that intrinsic bursters can create a more robust network with a wider range of output frequencies (Purvis et al 2007). …”

Section: Discussionmentioning

confidence: 99%

Two types of independent bursting mechanisms in inspiratory neurons: an integrative model

Toporikova¹,

Butera²

2010

J Comput Neurosci

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The network of coupled neurons in the pre-Bötzinger complex (pBC) of the medulla generates a bursting rhythm, which underlies the inspiratory phase of respiration. In some of these neurons, bursting persists even when synaptic coupling in the network is blocked and respiratory rhythmic discharge stops. Bursting in inspiratory neurons has been extensively studied, and two classes of bursting neurons have been identified, with bursting mechanism depends on either persistent sodium current or changes in intracellular Ca 2+ , respectively. Motivated by experimental evidence from these intrinsically bursting neurons, we present a two-compartment mathematical model of an isolated pBC neuron with two independent bursting mechanisms. Bursting in the somatic compartment is modeled via inactivation of a persistent sodium current, whereas bursting in the dendritic compartment relies on Ca 2+ oscillations, which are determined by the neuromodulatory tone. The model explains a number of conflicting experimental results and is able to generate a robust bursting rhythm, over a large range of parameters, with a frequency adjusted by neuromodulators.

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Section: Discussionmentioning

confidence: 99%

Two types of independent bursting mechanisms in inspiratory neurons: an integrative model

Toporikova¹,

Butera²

2010

J Comput Neurosci

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“…Mathematical models can be particularly helpful for generating experimentally testable hypotheses. A variety of models have been developed for the respiratory CPG [18,19,20,21,22,23,24,25], for chemosensory feedback-based regulation schemes [26,27,28], and for cardiopulmonary gas exchange [29]. See [30,31] for a review.…”

Section: Quantitative Modeling Approachmentioning

confidence: 99%

COVID-19 and silent hypoxemia in a minimal closed-loop model of the respiratory rhythm generator

Diekman

Thomas

Wilson

2023

Preprint

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Silent hypoxemia, or `happy hypoxia', is a puzzling phenomenon in which patients who have contracted COVID-19 exhibit very low oxygen saturation (SaO280%) but do not experience discomfort in breathing. The mechanism by which this blunted response to hypoxia occurs is unknown. We have previously shown that a computational model (Diekman et al., 2017, J. Neurophysiol) of the respiratory neural network can be used to test hypotheses focused on changes in chemosensory inputs to the central pattern generator (CPG). We hypothesize that altered chemosensory function at the level of the carotid bodies and/or the nucleus tractus solitarii are responsible for the blunted response to hypoxia. Here, we use our model to explore this hypothesis by altering the properties of the gain function representing oxygen sensing inputs to the CPG. We then vary other parameters in the model and show that oxygen carrying capacity is the most salient factor for producing silent hypoxemia. We call for clinicians to measure hematocrit as a clinical index of altered physiology in response to COVID-19 infection.

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COVID-19 and silent hypoxemia in a minimal closed-loop model of the respiratory rhythm generator

Diekman,

Thomas,

Wilson

2024

Biol Cybern

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Silent hypoxemia, or “happy hypoxia,” is a puzzling phenomenon in which patients who have contracted COVID-19 exhibit very low oxygen saturation ($$\text {SaO}_2$$ SaO 2 < 80%) but do not experience discomfort in breathing. The mechanism by which this blunted response to hypoxia occurs is unknown. We have previously shown that a computational model of the respiratory neural network (Diekman et al. in J Neurophysiol 118(4):2194–2215, 2017) can be used to test hypotheses focused on changes in chemosensory inputs to the central pattern generator (CPG). We hypothesize that altered chemosensory function at the level of the carotid bodies and/or the nucleus tractus solitarii are responsible for the blunted response to hypoxia. Here, we use our model to explore this hypothesis by altering the properties of the gain function representing oxygen sensing inputs to the CPG. We then vary other parameters in the model and show that oxygen carrying capacity is the most salient factor for producing silent hypoxemia. We call for clinicians to measure hematocrit as a clinical index of altered physiology in response to COVID-19 infection.

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Emergent Bursting in Small Networks of Model Conditional Pacemakers in the pre-Bötzinger Complex

Abstract: Abstract. This paper summarizes some lessons learned from the computational study of bursting oscillations in small networks of model pre-Bötzinger complex (pBC) neurons.

Cited by 3 publications

References 7 publications

Two types of independent bursting mechanisms in inspiratory neurons: an integrative model

Two types of independent bursting mechanisms in inspiratory neurons: an integrative model

COVID-19 and silent hypoxemia in a minimal closed-loop model of the respiratory rhythm generator

COVID-19 and silent hypoxemia in a minimal closed-loop model of the respiratory rhythm generator

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