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
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.