Bötzinger-complex expiratory neurons monosynaptically inhibit phrenic motoneurons in the decerebrate rat

1998 ◽  
Vol 122 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Guo-Feng Tian ◽  
John H. Peever ◽  
J. Duffin
Keyword(s):  
Phrenic Motoneurons ◽  
Bötzinger Complex ◽  
Decerebrate Rat ◽  
Expiratory Neurons

Morphology of expiratory neurons of the Bötzinger complex: An HRP study in the cat

1987 ◽  
Vol 258 (4) ◽  
pp. 565-579 ◽  
Author(s):  
Kazuyoshi Otake ◽  
Hiroshi Sasaki ◽  
Hajime Mannen ◽  
Kazuhisa Ezure
Keyword(s):  
Bötzinger Complex ◽  
Expiratory Neurons

Morphological characteristics of augmenting expiratory neurons of the Bötzinger complex

1987 ◽  
Vol 5 ◽  
pp. S20 ◽  
Author(s):  
Kazuyoshi Otake ◽  
Hiroshi Sasaki ◽  
Hajime Mannen ◽  
Kazuhisa Ezure ◽  
Motomu Manabe
Keyword(s):  
Morphological Characteristics ◽  
Bötzinger Complex ◽  
Expiratory Neurons

Decrementing expiratory neurons of the Bötzinger complex

1988 ◽  
Vol 72 (1) ◽  
pp. 150-158 ◽  
Author(s):  
M. Manabe ◽  
K. Ezure
Keyword(s):  
Bötzinger Complex ◽  
Expiratory Neurons

scholarly journals Inhibitory control of active expiration by the Bötzinger complex in rats

2019 ◽  
Author(s):  
Karine C. Flor ◽  
William H. Barnett ◽  
Marlusa Karlen-Amarante ◽  
Yaroslav Molkov ◽  
Daniel B. Zoccal
Keyword(s):  
Short Term ◽  
Inhibitory Circuitry ◽  
Respiratory Network ◽  
Bötzinger Complex ◽  
Expiratory Neurons ◽  
Parafacial Respiratory Group ◽  
And Control ◽  
Pharmacological Manipulations ◽  
Sustained Hypoxia

ABSTRACTThe expiratory neurons of the Bötzinger complex (BötC) provide inhibitory inputs to the respiratory network, which, during eupnea, are critically important for respiratory phase transition and duration control. Herein, we investigated how the BötC neurons interact with the expiratory oscillator located in the parafacial respiratory group (pFRG) and control the abdominal activity during active expiration. Using the decerebrated, arterially perfused in situ rat preparations, we recorded the neuronal activity and performed pharmacological manipulations of the BötC and pFRG during hypercapnia or after the exposure to short-term sustained hypoxia – conditions that generate active expiration. The experimental data were integrated in a mathematical model to gain new insights in the inhibitory connectome within the respiratory central pattern generator. Our results reveal a complex inhibitory circuitry within the BötC that provides inhibitory inputs to the pFRG thus restraining abdominal activity under resting conditions and contributing to abdominal expiratory pattern formation during active expiration.

scholarly journals Respiratory responses to thyrotropin-releasing hormone microinjected into the rabbit medulla oblongata

1999 ◽  
Vol 277 (5) ◽  
pp. R1331-R1338 ◽  
Author(s):  
Donatella Mutolo ◽  
Fulvia Bongianni ◽  
Marco Carfì ◽  
Tito Pantaleo
Keyword(s):  
Area Postrema ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Dorsal Respiratory Group ◽  
Bötzinger Complex ◽  
Expiratory Neurons ◽  
Inspiratory Activity ◽  
First Time ◽  
Respiratory Responses

We investigated the respiratory role of thyrotropin-releasing hormone (TRH) input to medullary structures involved in the control of breathing in anesthetized, vagotomized, paralyzed, and artificially ventilated rabbits. Microinjections (10–20 nl) of 1 or 10 mM TRH were performed in different regions of the ventral respiratory group (VRG), namely the rostral expiratory portion or Bötzinger complex (Böt. c.), the inspiratory portion, the transition zone between these two neuronal pools, and the caudal expiratory component. TRH microinjections were also performed in the dorsal respiratory group (DRG) and the area postrema (AP). Injection sites were localized by using stereotaxic coordinates and extracellular recordings of neuronal activity; their locations were confirmed by subsequent histological control. TRH microinjections in the Böt. c. and the directly caudally located region where a mix of inspiratory and expiratory neurons were encountered elicited depressant respiratory responses. TRH microinjections were completely ineffective at sites within the inspiratory and the caudal expiratory components of the VRG. TRH microinjections in either the DRG or the AP induced excitatory effects on inspiratory activity. The results show for the first time that TRH may exert inhibitory influences on respiration at medullary levels by acting on rostral expiratory neurons and that not only the DRG, as previously suggested, but also the AP may mediate TRH-induced excitatory effects on respiration.

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