α1-Adrenergic receptor-induced slow rhythmicity in nonrespiratory cervical motoneurons of neonatal rat spinal cord
European Journal of Neuroscience. 2000-08-01; 12(8): 2950-2966
DOI: 10.1046/j.1460-9568.2000.00154.x
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1. Eur J Neurosci. 2000 Aug;12(8):2950-66.
alpha1-adrenergic receptor-induced slow rhythmicity in nonrespiratory cervical
motoneurons of neonatal rat spinal cord.
Morin D(1), Bonnot A, Ballion B, Viala D.
Author information:
(1)Laboratoire de Neurobiologie des Réseaux, UMR CNRS 5816, Université Bordeaux
1, avenue des Facultés, 33405 Talence Cedex, France.
Previous studies have reported that the alpha1-adrenergic system can activate
spinal rhythm generators belonging to the central respiratory network. In order
to analyse alpha1-adrenergic effects on both cranial and spinal motoneuronal
activity, phenylephrine (1-800 microM) was applied to in vitro preparations of
neonatal rat brainstem-spinal cord. High concentration of phenylephrine
superfusion exerted multiple effects on spinal cervical outputs (C2-C6),
consisting of a lengthening of respiratory period and an increase in inspiratory
burst duration. Furthermore, in 55% of cases a slow motor rhythm recorded from
the same spinal outputs was superimposed on the inspiratory activity. However,
this phenylephrine-induced slow motor rhythm generated at the spinal level was
observed neither in inspiratory cranial nerves (glossopharyngeal, vagal and
hypoglossal outputs) nor in phrenic nerves. Whole-cell patch-clamp recordings
were carried out on cervical motoneurons (C4-C5), to determine first which
motoneurons were involved in this slow rhythm, and secondly the cellular events
underlying direct phenylephrine effects on motoneurons. In all types of
motoneurons (inspiratory and nonrespiratory) phenylephrine induced a prolonged
depolarization with an increase in neuronal excitability. However, only
nonrespiratory motoneurons showed additional rhythmic membrane depolarizations
(with spiking) occurring in phase with the slow motor rhythm recorded from the
ventral root. Furthermore the tonic depolarization produced in all motoneurons
results from an inward current [which persists in the presence of tetrodotoxin
(TTX)] associated with a decrease in neuron input conductance, with a reversal
potential varying as a Nernstian function of extracellular K+ concentration. Our
results indicate that the alpha1-adrenoceptor activation: (i) affects both the
central respiratory command (i.e. respiratory period and inspiratory burst
duration) and spinal inspiratory outputs; (ii) induces slow spinal motor
rhythmicity, which is unlikely to be related to the respiratory system; and
(iii), increases motoneuronal excitability, probably through a decrease in
postsynaptic leak K+ conductance.
DOI: 10.1046/j.1460-9568.2000.00154.x
PMID: 10971636 [Indexed for MEDLINE]