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Murine Carotid Body Responses to Hypoxia: In vivo Carotid Sinus Nerve Recordings in the DBA/2J and A/J Strains.
Author(s) -
Pichard Luis,
Sgambati Francis,
Kostuk Eric,
Bashai Pejmon,
Fitzgerald Robert,
Shirahata Machiko
Publication year - 2010
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.24.1_supplement.1026.19
Subject(s) - carotid body , hypoxia (environmental) , in vivo , carotid sinus , glomus cell , cardiorespiratory fitness , chemistry , medicine , anesthesia , anatomy , endocrinology , electrophysiology , biology , oxygen , blood pressure , microbiology and biotechnology , organic chemistry
The role of the carotid body (CB) as a primary chemosensor is well established in large mammals. Due to our ability to better modify the genome the mouse has been used for hypoxic chemosensing research. The only method by which one can study the global and unified CB response to hypoxia is via recording the carotid sinus nerve (CSN) activity. Our laboratory has been using the two inbred strains of mice, DBA/2J and A/J. In general, the DBA/2J is more sensitive, with an elevated cardiorespiratory response to hypoxia compared to the A/J strain. Thus, the purpose of this study is to establish a stable in vivo model for recording CSN activity in these two strains of mice. CSN activity was recorded from the central end just prior to its junction to the glossopharyngeal nerve using a glass suction pipette in six DBA/2J and A/J mice. Baroreceptor activity was mechanically disrupted. Following a baseline recording, the inspired gases were changed from hyperoxia to F I O2=0.21, 0.15 and 0.10. CSN activity was then analyzed using Fast Fourier Transform (FFT) based time‐frequency spectral analysis. The data showed a hyperbolic relationship between PO2 and CSN activity in the DBA/2J mice. The A/J mice showed a significant attenuation in their carotid body neural output when compared to the DBA/2J mouse at all comparable levels of normoxia and hypoxia. Thus, the model established methods to examine carotid body responses to hypoxia in mice and showed a clear difference in the carotid body generated neural output in the DBA/2J mouse when compared to the A/J. This model can now be used to study how the different genetic make‐up, by using other strains and knockouts, can alter the overall in‐vivo response to hypoxia. Support: F31HL096450, HL081345 , AHA 09GRNT2080158, HL50712 and HL61596.