scholarly journals Mechanism of central hypopnoea induced by organic phosphorus poisoning

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kazuhito Nomura ◽  
Eichi Narimatsu ◽  
Hiroyuki Inoue ◽  
Ryoko Kyan ◽  
Keigo Sawamoto ◽  
...  
Keyword(s):  
Respiratory Burst ◽  
Organic Phosphorus ◽  
Acetylcholinesterase Inhibitor ◽  
Respiratory Rhythm ◽  
Electrode Array ◽  
Brainstem Slice ◽  
Toxicological Studies ◽  
Bötzinger Complex ◽  
Central Apnoea ◽  
Multi Electrode Array

Abstract Whether central apnoea or hypopnoea can be induced by organophosphorus poisoning remains unknown to date. By using the acute brainstem slice method and multi-electrode array system, we established a paraoxon (a typical acetylcholinesterase inhibitor) poisoning model to investigate the time-dependent changes in respiratory burst amplitudes of the pre-Bötzinger complex (respiratory rhythm generator). We then determined whether pralidoxime or atropine, which are antidotes of paraoxon, could counteract the effects of paraoxon. Herein, we showed that paraoxon significantly decreased the respiratory burst amplitude of the pre-Bötzinger complex (p < 0.05). Moreover, pralidoxime and atropine could suppress the decrease in amplitude by paraoxon (p < 0.05). Paraoxon directly impaired the pre-Bötzinger complex, and the findings implied that this impairment caused central apnoea or hypopnoea. Pralidoxime and atropine could therapeutically attenuate the impairment. This study is the first to prove the usefulness of the multi-electrode array method for electrophysiological and toxicological studies in the mammalian brainstem.

scholarly journals Patch-clamp and multi-electrode array electrophysiological analysis in acute mouse brain slices

2021 ◽  
Vol 2 (2) ◽  
pp. 100442
Author(s):  
Kevin M. Manz ◽  
Justin K. Siemann ◽  
Douglas G. McMahon ◽  
Brad A. Grueter
Keyword(s):  
Patch Clamp ◽  
Mouse Brain ◽  
Brain Slices ◽  
Electrode Array ◽  
Electrophysiological Analysis ◽  
Multi Electrode Array

Pre-Bötzinger Complex Functions as a Central Hypoxia Chemosensor for Respiration In Vivo

2000 ◽  
Vol 83 (5) ◽  
pp. 2854-2868 ◽  
Author(s):  
Irene C. Solomon ◽  
Norman H. Edelman ◽  
Judith A. Neubauer
Keyword(s):  
Short Duration ◽  
Phrenic Nerve ◽  
Excitatory Amino Acid ◽  
Respiratory Rhythm ◽  
High Amplitude ◽  
Unique Region ◽  
Homocysteic Acid ◽  
Bötzinger Complex ◽  
Nerve Discharge

Recently, we identified a region located in the pre-Bötzinger complex (pre-BötC; the proposed locus of respiratory rhythm generation) in which activation of ionotropic excitatory amino acid receptors usingdl-homocysteic acid (DLH) elicits a variety of excitatory responses in the phrenic neurogram, ranging from tonic firing to a rapid series of high-amplitude, rapid rate of rise, short-duration inspiratory bursts that are indistinguishable from gasps produced by severe systemic hypoxia. Therefore we hypothesized that this unique region is chemosensitive to hypoxia. To test this hypothesis, we examined the response to unilateral microinjection of sodium cyanide (NaCN) into the pre-BötC in chloralose- or chloralose/urethan-anesthetized vagotomized, paralyzed, mechanically ventilated cats. In all experiments, sites in the pre-BötC were functionally identified using DLH (10 mM, 21 nl) as we have previously described. All sites were histologically confirmed to be in the pre-BötC after completion of the experiment. Unilateral microinjection of NaCN (1 mM, 21 nl) into the pre-BötC produced excitation of phrenic nerve discharge in 49 of the 81 sites examined. This augmentation of inspiratory output exhibited one of the following changes in cycle timing and/or pattern: 1) a series of high-amplitude, short-duration bursts in the phrenic neurogram (a discharge similar to a gasp), 2) a tonic excitation of phrenic neurogram output, 3) augmented bursts in the phrenic neurogram (i.e., eupneic breath ending with a gasplike burst), or 4) an increase in frequency of phrenic bursts accompanied by small increases or decreases in the amplitude of integrated phrenic nerve discharge. Our findings identify a locus in the brain stem in which focal hypoxia augments respiratory output. We propose that the respiratory rhythm generator in the pre-BötC has intrinsic hypoxic chemosensitivity that may play a role in hypoxia-induced gasping.

Models of Respiratory Rhythm Generation in the Pre-Bötzinger Complex. I. Bursting Pacemaker Neurons

1999 ◽  
Vol 82 (1) ◽  
pp. 382-397 ◽  
Author(s):  
Robert J. Butera ◽  
John Rinzel ◽  
Jeffrey C. Smith
Keyword(s):  
Membrane Potential ◽  
Respiratory Rhythm ◽  
Rhythm Generation ◽  
Minimal Models ◽  
Dynamic Features ◽  
Bursting Neurons ◽  
Wide Range ◽  
Bötzinger Complex ◽  
Voltage Dependent ◽  
Respiratory Rhythm Generation

A network of oscillatory bursting neurons with excitatory coupling is hypothesized to define the primary kernel for respiratory rhythm generation in the pre-Bötzinger complex (pre-BötC) in mammals. Two minimal models of these neurons are proposed. In model 1, bursting arises via fast activation and slow inactivation of a persistent Na+ current I NaP-h. In model 2, bursting arises via a fast-activating persistent Na+ current INaP and slow activation of a K+ current IKS. In both models, action potentials are generated via fast Na+ and K+currents. The two models have few differences in parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms. Both models are consistent with many of the dynamic features of electrophysiological recordings from pre-BötC oscillatory bursting neurons in vitro, including voltage-dependent activity modes (silence, bursting, and beating), a voltage-dependent burst frequency that can vary from 0.05 to >1 Hz, and a decaying spike frequency during bursting. These results are robust and persist across a wide range of parameter values for both models. However, the dynamics of model 1 are more consistent with experimental data in that the burst duration decreases as the baseline membrane potential is depolarized and the model has a relatively flat membrane potential trajectory during the interburst interval. We propose several experimental tests to demonstrate the validity of either model and to differentiate between the two mechanisms.

scholarly journals Influence of Electric Current and Magnetic Flow on Firing Patterns of Pre-Bötzinger Complex Model

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Wenchao Ji ◽  
Moutian Liu ◽  
Lixia Duan
Keyword(s):  
Electric Current ◽  
Respiratory Rhythm ◽  
Complex Model ◽  
Neuronal Firing ◽  
Essential Factor ◽  
Firing Activity ◽  
Magnetic Flow ◽  
Bötzinger Complex ◽  
Bistable Structure ◽  
Slow Decomposition

The dynamics of neuronal firing activity is vital for understanding the pathological respiratory rhythm. Studies on electrophysiology show that the magnetic flow is an essential factor that modulates the firing activities of neurons. By adding the magnetic flow to Butera’s neuron model, we investigate how the electric current and magnetic flow influence neuronal activities under certain parametric restrictions. Using fast-slow decomposition and bifurcation analysis, we show that the variation of external electric current and magnetic flow leads to the change of the bistable structure of the system and hence results in the switch of neuronal firing pattern from one type to another.

scholarly journals Conductive hybrid carbon nanotube (CNT)–polythiophene coatings for innovative auditory neuron-multi-electrode array interfacing

RSC Advances ◽  
2016 ◽  
Vol 6 (48) ◽  
pp. 41714-41723 ◽  
Author(s):  
S. Ostrovsky ◽  
S. Hahnewald ◽  
R. Kiran ◽  
P. Mistrik ◽  
R. Hessler ◽  
...  
Keyword(s):  
Surface Modification ◽  
Carbon Nanotube ◽  
Cochlear Implants ◽  
Electrode Array ◽  
Auditory Neuron ◽  
Platinum Electrodes ◽  
Electrode Interface ◽  
Conductive Properties ◽  
Hybrid Carbon ◽  
Multi Electrode Array

Surface modification of platinum electrodes to improve neuron-electrode interface and electrode conductive properties in cochlear implants.

scholarly journals Lethal avian influenza A (H5N1) virus induces ataxic breathing in mice with apoptosis of pre-Botzinger complex neurons expressing neurokinin-1 receptor

2017 ◽  
Vol 313 (5) ◽  
pp. L772-L780 ◽  
Author(s):  
Jianguo Zhuang ◽  
Na Zang ◽  
Chunyan Ye ◽  
Fadi Xu
Keyword(s):  
Respiratory Failure ◽  
Influenza A ◽  
Early Stage ◽  
Respiratory Rhythm ◽  
Body Weight Loss ◽  
Neurokinin 1 Receptor ◽  
Arterial Blood ◽  
Bötzinger Complex ◽  
Neurokinin 1 ◽  
Active Caspase

Lethal influenza A (H5N1) induces respiratory failure in humans. Although it also causes death at 7 days postinfection (dpi) in mice, the development of the respiratory failure and the viral impact on pre-Botzinger complex (PBC) neurons expressing neurokinin 1 receptor (NK1R), which is the respiratory rhythm generator, have not been explored. Body temperature, weight, ventilation, and arterial blood pH and gases were measured at 0, 2, 4, and 6 dpi in control, lethal HK483, and nonlethal HK486 viral-infected mice. Immunoreactivities (IR) of PBC NK1R, H5N1 viral nucleoprotein (NP), and active caspase-3 (CASP3; a marker for apoptosis) were detected at 6 dpi. HK483, but not HK486, mice showed the following abnormalities: 1) gradual body weight loss and hypothermia; 2) tachypnea at 2–4 dpi and ataxic breathing with long-lasting apneas and hypercapnic hypoxemia at 6 dpi; and 3) viral replication in PBC NK1R neurons with NK1R-IR reduced by 75% and CASP3-IR colabeled at 6 dpi. Lethal H5N1 viral infection causes tachypnea at the early stage and ataxic breathing and apneas (hypercapnic hypoxemia) leading to death at the late stage. Its replication in the PBC induces apoptosis of local NK1R neurons, contributing to ataxic breathing and respiratory failure.

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