Neuroscience 2000 Abstract
| Presentation Number: | 546.7 |
|---|---|
| Abstract Title: | Glycinergic inhibition is critical for upper airway control in the <I>in situ</I> neonatal rat working-heart brainstem preparation. |
| Authors: |
Dutschmann, M.*2
; Schmid, S.1
; Paton, J. F. R.2
1Animal Physiology, University of Tübingen, Tübingen, Germany 2Physiology, University of Bristol, Bristol, United Kingdom |
| Primary Theme and Topics |
E. Endocrine and Autonomic Regulation - 69. Respiratory regulation |
| Secondary Theme and Topics | E. Endocrine and Autonomic Regulation<br />- 66. Cardiovascular regulation: central control |
| Session: |
546. Respiratory regulation: motor output and reflexes Poster |
| Presentation Time: | Tuesday, November 7, 2000 3:00 PM-4:00 PM |
| Location: | Hall G-J |
| Keywords: | respiratory, development, SIDS, rhythm generation |
Recent in vitro studies reported that glycinergic inhibition was not necessary for respiratory rhythm generation in neonatal rats. Due to the limitations of these preparations there are no data regarding a potential role for central glycinergic mechanisms controlling the upper airways. In the present study, we used the arterially perfused WHBP of neonatal rats (P0-P4) which allows both kineisiological and cellular studies (see: SFN abstr. Paton et al.: Respiratory activity in the neonatal rat). To determine a role for glycinergic inhibition in upper airway control we recorded recurrent laryngeal nerve activity as an index of motor output to the glottis before and after administration of strychnine (0.5-1.5µM) to the perfusate. Strychnine caused post-inspiratory activity to shift towards the inspiratory phase (n=8). Functionally, as revealed by measuring changes in laryngeal resistance (n=7), strychnine converted the normal inspiratory glottic dilatation (seen during control) to a constriction. Exposing post-inspiratory neurones (extra: n= 8; intra; n=4) to strychnine revealed: (i) a loss of inspiratory inhibition and, (ii) firing during the inspiratory phase of the respiratory cycle. We conclude that glycinergic inhibition in the respiratory network of neonatal rats is essential for the maintenance of upper airway patency and generation of eupnoea. Developmental disorders of glycinergic mechanisms might play a critical role in sudden infant death syndrome and obstructive breathing disorders.
Supported by the British Heart Foundation & Deutsche Forschungsgemeinschaft.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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