THE ADRENERGIC MODULATION OF FIRINGS OF RESPIRATORY RHYTHM-GENERATINGNEURONS IN MEDULLA-SPINAL CORD PREPARATION FROM NEWBORN RAT

Citation
A. Arata et al., THE ADRENERGIC MODULATION OF FIRINGS OF RESPIRATORY RHYTHM-GENERATINGNEURONS IN MEDULLA-SPINAL CORD PREPARATION FROM NEWBORN RAT, Experimental Brain Research, 119(4), 1998, pp. 399-408
Citations number
41
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144819
Volume
119
Issue
4
Year of publication
1998
Pages
399 - 408
Database
ISI
SICI code
0014-4819(1998)119:4<399:TAMOFO>2.0.ZU;2-V
Abstract
We analysed the modulation of respiratory neurons by adrenaline or nor adrenaline (NA) in a newborn rat brainstem-spinal cord preparation. Ad renaline or NA caused a dose-dependent depression of the respiratory r hythm and induced C4 spinal tonic discharges. The inhibitory effect of adrenaline (ED50=0.5 mu M) on the respiratory rhythm was stronger tha n NA (ED50=5 mu M) The adrenaline respiratory rhythm depression was pa rtially blocked by the alpha(1)-antagonist prazosin or by the alpha(2) -antagonist yohimbine. The C4 tonic discharge elicited by adrenaline w as blocked by the alpha(1)-antagonist prazosin. The direct effects of adrenaline on pre-inspiratory (Pre-I) neurons were examined in a synap tic blockade solution (low Ca), and fifty-six percent of Pre-I neurons were found to continue firing. In low-Ca solution, Pre-I neurons were excited (n=29 of 39) or depressed (n=5 of 39) by adrenaline, and exci ted by alpha(1)-agonist phenylephrine or depressed by alpha(2)-agonist clonidine. These results suggest that the respiratory rhythm depressi on under intact network conditions is mediated by some other inhibitor y system. The inhibitory effect of adrenaline on the respiratory rhyth m was partially blocked by the GABA(A)-antagonists bicuculline or picr otoxin, but not by the GABA(B)-antagonist phaclofen. The present resul ts suggest that: (1) respiratory rhythm generation is more sensitive t o adrenaline than NA through alpha-adrenergic action of adrenaline; (2 ) the activity of Pre-I neurons could be directly regulated by excitat ion via alpha(1)-receptors and inhibition via alpha(2)-receptors; and (3) the depression of the respiratory rhythm by adrenaline is partly m ediated by GABA(A)ergic neurons.