Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 162, Issue 1, Pages 41-47Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.resp.2008.03.013
Keywords
respiration; intracellular recording; drug iontophoresis
Categories
Ask authors/readers for more resources
Laryngeal constrictor motoneurons (LCMN) are activated during post-inspiration and act to slow expiratory airflow. However, little is known about how this phasic activity is generated. Here, we investigated the electrophysiological responses of identified LCMN to local application of GABA and bicuculline methiodide (BIC) in 14 anaesthetised Sprague-Dawley rats. During extracellular recordings, GABA iontophoresis (0.5 M) strongly inhibited LCMN (n=6). Interestingly, BIC iontophoresis (5 mM) reduced, rather than increased, LCMN post-inspiratory activity (5 out of 6). Furthermore, intracellular recording revealed that BIC reduced not only the hyperpolarisation of the LCMN during inspiration (2.5 +/- 1.4 mV before and 1.5 +/- 0.4 mV after the BIC, P=0.05, n = 5), but also the depolarisation during post-inspiration (3.0 +/- 1.3 mV before and 1.6 +/- 0.4 mV after the BIC, P=0.02, n=5). Our results demonstrate for the first time that the inspiratory inhibition of LCMN is primarily mediated by GABA(A) receptors. A possible involvement of a post-inhibitory rebound mechanism is discussed to explain how blockade of an inspiratory inhibition would affect LCMN excitability during post-inspiration. (c) 2008 Published by Elsevier B.V.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available