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The Journal of Neuroscience, April 18, 2007, 27(16):4435-4442; doi:10.1523/JNEUROSCI.2803-06.2007

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Cellular/Molecular
Episodic Stimulation of 1-Adrenoreceptors Induces Protein Kinase C-Dependent Persistent Changes in Motoneuronal Excitability

Natalia V. Neverova,¹ Shane A. Saywell,¹ Lisa J. Nashold,² Gordon S. Mitchell,^1,2 and Jack L. Feldman¹

¹Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095-1763, and ²Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin 53706

Correspondence should be addressed to Jack L. Feldman, Department of Neurobiology, David Geffen School of Medicine at University of California, Los Angeles, Box 951763, Los Angeles, CA 90095-1763. Email: feldman{at}ucla.edu

In vitro long-term facilitation (ivLTF) is a novel form of activity-independent postsynaptic enhancement of AMPA receptor function in hypoglossal (XII) motoneurons that can be induced by intermittent activation of 5-HT₂ receptors. In vivo respiratory long-term facilitation (LTF) is characterized by a persistent 5-HT₂ receptor-dependent increase in respiratory motor output or ventilation after episodic exposures to hypoxia in adult rats. Here, we demonstrate that ivLTF can also be induced by episodic but not continuous stimulation of 1-adrenergic receptors that requires protein kinase C (PKC), but not PKA (protein kinase A), activation. Additionally, we show that in vivo respiratory LTF is also 1-adrenergic receptor dependent. We suggest that, in vivo, concurrent episodic activation of 5-HT₂ and 1-adrenergic receptors is necessary to produce long-lasting changes in the excitability of respiratory motoneurons, possibly involving PKC activation via the G_q–PLC (phospholipase C) signaling pathway common to both receptor subtypes. Such plasticity of XII motor output may increase upper airway muscle (innervated by XII nerve) tone and improve the likelihood that airway patency will be maintained. Elucidating the mechanism underlying LTF can be of clinical importance to the patients suffering from sleep-disordered breathing.

Key words: long-term facilitation (LTF); plasticity; respiration; PKC; motoneuron; adrenergic

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Received Aug. 16, 2004; revised Feb. 22, 2007; accepted March 16, 2007.

Correspondence should be addressed to Jack L. Feldman, Department of Neurobiology, David Geffen School of Medicine at University of California, Los Angeles, Box 951763, Los Angeles, CA 90095-1763. Email: feldman{at}ucla.edu

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