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Articles in PresS, published online ahead of print December 21, 2001
J Appl Physiol, 10.1152/jap.00475.2001
Submitted on May 17, 2001
Accepted on December 14, 2001
* To whom correspondence should be addressed. E-mail: g.miles{at}auckland.ac.nz.
Based on the high level of P2X receptor expression on phrenic motoneurons (MNs) in rat (23), and potentiation of XII MN inspiratory activity by ATP (15), we tested the hypothesis that ATP receptor activation also modulates phrenic MN activity. This question was examined in rhythmically-active brainstem-spinal cord preparations from neonatal rats by monitoring effects of ATP on the activity of the spinal C4 root and phrenic MNs. ATP produced a rapid-onset, dose-dependent, suramin- and PPADS-sensitive increase in C4 root tonic discharge and a 22±7% potentiation of inspiratory burst amplitude. This was followed by a slower, 10±5% reduction in burst amplitude. ATP-
-s, the hydrolysis-resistant analogue, evoked only the excitatory response. ATP induced inward currents (57±39pA) and increased repetitive firing of phrenic MNs. These data, combined with persistence of ATP currents in TTX and immunolabelling for P2X2 receptors in Fluoro-Gold labelled C4 MNs, implicate postsynaptic P2 receptors in the excitation. Inspiratory synaptic currents, however, were inhibited by ATP. This inhibition differed from that seen in root recordings; it did not follow an excitation, had a faster onset, and was induced by ATP--s. Thus, ATP inhibited activity through at least two mechanisms: i) a rapid P2 receptor-mediated inhibition; and ii) a delayed P1 receptor-mediated inhibition associated with hydrolysis of ATP to adenosine. The complex effects of ATP on phrenic MNs highlight the importance of ATP as a modulator of central motor outflows.
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