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Increasing or decreasing the excitability of V2a neurons activates accessory respiratory muscles
Author(s) -
Jensen Victoria N.,
Seedle Kari,
Turner Sarah M.,
Crone Steven A.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.893.2
Subject(s) - muscles of respiration , brainstem , excitatory postsynaptic potential , respiratory system , spinal cord , medicine , glutamatergic , diaphragm (acoustics) , neuroscience , respiration , ventilation (architecture) , inhibitory postsynaptic potential , electromyography , anesthesia , anatomy , biology , glutamate receptor , physical medicine and rehabilitation , physics , receptor , acoustics , loudspeaker , mechanical engineering , engineering
Accessory respiratory muscles (ARMs) can be recruited to maintain respiration when the diaphragm is impaired or weakened, such as patients with Amyotrophic Lateral Sclerosis (ALS) or spinal cord injury. We chronically record mouse diaphragm electromyography (EMG), ARM EMG, and whole body plethysmography to assess the effect of activating and silencing V2a neurons with DREADDs on respiratory muscle activity and ventilation. Increasing the excitability of glutamatergic V2a neurons in the brainstem and/or the spinal cord recruits ARMs and enhances ventilation. Interestingly, silencing V2a neurons also activates ARMs. We hypothesize that V2a neurons participate in both excitatory and inhibitory pathways controlling activation of ARMs for breathing. Support or Funding Information University of Cincinnati T32 Training Grant 2016–2017 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .