scholarly journals ATP sensitivity of preBötzinger complex neurones in neonatal ratin vitro: mechanism underlying a P2 receptor-mediated increase in inspiratory frequency

2008 ◽  
Vol 586 (5) ◽  
pp. 1429-1446 ◽  
Author(s):  
A. R. Lorier ◽  
J. Lipski ◽  
G. D. Housley ◽  
J. J. Greer ◽  
G. D. Funk
Keyword(s):  
P2 Receptor ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

scholarly journals Normal breathing requires preBötzinger complex neurokinin-1 receptor-expressing neurons

2001 ◽  
Vol 4 (9) ◽  
pp. 927-930 ◽  
Author(s):  
Paul A. Gray ◽  
Wiktor A. Janczewski ◽  
Nicholas Mellen ◽  
Donald R. McCrimmon ◽  
Jack L. Feldman
Keyword(s):  
Neurokinin 1 Receptor ◽  
Normal Breathing ◽  
Neurokinin 1 ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

cAMP‐dependent modulation of I h underlies the P2Y 1 receptor‐mediated excitation of the preBötzinger Complex inspiratory network in vitro

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Yong Zhang ◽  
Vivian Biancardi ◽  
Ana Miranda Tapia ◽  
Toka Abu Jaib ◽  
Alexander Gourine ◽  
...  
Keyword(s):  
Prebotzinger Complex ◽  
Prebötzinger Complex

scholarly journals Mechanisms Underlying Regulation of Respiratory Pattern by Nicotine in PreBötzinger Complex

2001 ◽  
Vol 85 (6) ◽  
pp. 2461-2467 ◽  
Author(s):  
Xuesi M. Shao ◽  
Jack L. Feldman
Keyword(s):  
Respiratory Frequency ◽  
Neonatal Rat ◽  
Respiratory Pattern ◽  
Dependent Manner ◽  
Baseline Noise ◽  
Arterial Blood ◽  
Inspiratory Neurons ◽  
Excitatory Neurotransmission ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

Cholinergic neurotransmission plays a role in regulation of respiratory pattern. Nicotine from cigarette smoke affects respiration and is a risk factor for sudden infant death syndrome (SIDS) and sleep-disordered breathing. The cellular and synaptic mechanisms underlying this regulation are not understood. Using a medullary slice preparation from neonatal rat that contains the preBötzinger Complex (preBötC), the hypothesized site for respiratory rhythm generation, and generates respiratory-related rhythm in vitro, we examined the effects of nicotine on excitatory neurotransmission affecting inspiratory neurons in preBötC and on the respiratory-related motor activity from hypoglossal nerve (XIIn). Microinjection of nicotine into preBötC increased respiratory frequency and decreased the amplitude of inspiratory bursts, whereas when injected into XII nucleus induced a tonic activity and an increase in amplitude but not in frequency of inspiratory bursts from XIIn. Bath application of nicotine (0.2–0.5 μM, approximately the arterial blood nicotine concentration immediately after smoking a cigarette) increased respiratory frequency up to 280% of control in a concentration-dependent manner. Nicotine decreased the amplitude to 82% and increased the duration to 124% of XIIn inspiratory bursts. In voltage-clamped preBötC inspiratory neurons (including neurons with pacemaker properties), nicotine induced a tonic inward current of −19.4 ± 13.4 pA associated with an increase in baseline noise. Spontaneous excitatory postsynaptic currents (sEPSCs) present during the expiratory period increased in frequency to 176% and in amplitude to 117% of control values; the phasic inspiratory drive inward currents decreased in amplitude to 66% and in duration to 89% of control values. The effects of nicotine were blocked by mecamylamine (Meca). The inspiratory drive current and sEPSCs were completely eliminated by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in the presence or absence of nicotine. In the presence of tetrodotoxin (TTX), low concentrations of nicotine did not induce any tonic current or any increase in baseline noise, nor affect the input resistance in inspiratory neurons. In this study, we demonstrated that nicotine increased respiratory frequency and regulated respiratory pattern by modulating the excitatory neurotransmission in preBötC. Activation of nicotinic acetylcholine receptors (nAChRs) enhanced the tonic excitatory synaptic input to inspiratory neurons including pacemaker neurons and at the same time, inhibited the phasic excitatory coupling between these neurons. These mechanisms may account for the cholinergic regulation of respiratory frequency and pattern.

scholarly journals Exploring opioid receptor dependent biased agonism in the PreBötzinger Complex

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Caroline C. Szujewski ◽  
Chrishon Campbell ◽  
Alfredo J. Garcia
Keyword(s):  
Opioid Receptor ◽  
Biased Agonism ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

scholarly journals Neuronal Mediators of the Frequency Increase Evoked by Activation of P2Y 1 Receptors in the preBötzinger Complex Inspiratory Rhythm Generating Network in Vitro

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Ana Miranda Tapia ◽  
Vivian Biancardi ◽  
Robert Reklow ◽  
Wei Zhang ◽  
Vladimir Rancic ◽  
...  
Keyword(s):  
Frequency Increase ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex

scholarly journals Muscarinic Modulation of Morphologically Identified Glycinergic Neurons in the Mouse PreBötzinger Complex

2020 ◽  
Vol 13 ◽  
Author(s):  
Fang Zheng ◽  
Barbara E. Nixdorf-Bergweiler ◽  
Elke Edelmann ◽  
Johannes F. M. van Brederode ◽  
Christian Alzheimer
Keyword(s):  
Prebotzinger Complex ◽  
Prebötzinger Complex ◽  
Muscarinic Modulation

scholarly journals Multi-Level Regulation of Opioid-Induced Respiratory Depression

Physiology ◽  
2020 ◽  
Vol 35 (6) ◽  
pp. 391-404
Author(s):  
Barbara Palkovic ◽  
Vitaliy Marchenko ◽  
Edward J. Zuperku ◽  
Eckehard A. E. Stuth ◽  
Astrid G. Stucke
Keyword(s):  
Respiratory Rate ◽  
Respiratory Depression ◽  
Minute Ventilation ◽  
Direct Effects ◽  
Respiratory Phase ◽  
Multi Level ◽  
Prebotzinger Complex ◽  
Prebötzinger Complex ◽  
Excitatory Drive

Opioids depress minute ventilation primarily by reducing respiratory rate. This results from direct effects on the preBötzinger Complex as well as from depression of the Parabrachial/Kölliker-Fuse Complex, which provides excitatory drive to preBötzinger Complex neurons mediating respiratory phase-switch. Opioids also depress awake drive from the forebrain and chemodrive.

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