Adrenergic alpha(1) receptor activation is sufficient, but not necessary for phrenic long-term facilitation

作者：Huxtable A G; MacFarlane P M; Vinit S; Nichols N L; Dale E A; Mitchell G S^*

来源：Journal of Applied Physiology, 2014, 116(11): 1345-1352.

DOI：10.1152/japplphysiol.00904.2013

• spinal cord
• alpha(1) receptors
• plasticity
• respiratory motor neuron

Acute intermittent hypoxia (AIH; three 5-min hypoxic episodes) causes a form of phrenic motor facilitation (pMF) known as phrenic long-term facilitation (pLTF); pLTF is initiated by spinal activation of Gq protein-coupled 5-HT2 receptors. Because alpha(1) adrenergic receptors are expressed in the phrenic motor nucleus and are also Gq protein-coupled, we hypothesized that alpha(1) receptors are sufficient, but not necessary for AIH-induced pLTF. In anesthetized, paralyzed, and ventilated rats, episodic spinal application of the alpha(1) receptor agonist phenylephrine (PE) elicited dose-dependent pMF (10 and 100 mu M, P < 0.05; but not 1 mu M). PE-induced pMF was blocked by the alpha(1) receptor antagonist prazosin (1 mM; -20 +/- 20% at 60 min, -5 +/- 21% at 90 min; n = 6). Although alpha(1) receptor activation is sufficient to induce pMF, it was not necessary for AIH-induced pLTF because intrathecal prazosin (1 mM) did not alter AIH-induced pLTF (56 +/- 9% at 60 min, 78 +/- 12% at 90 min; n = 9). Intravenous (iv) prazosin (150 mu g/kg) appeared to reduce pLTF (21 +/- 9% at 60 min, 26 +/- 8% at 90 min), but this effect was not significant. Hypoglossal long-term facilitation was unaffected by intrathecal prazosin, but was blocked by iv prazosin (-4 +/- 14% at 60 min, -13 +/- 18% at 90 min), suggesting different LTF mechanisms in different motor neuron pools. In conclusion, Gq protein-coupled alpha(1) adrenergic receptors evoke pMF, but they are not necessary for AIH-induced pLTF.

• 出版日期2014-6