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Episodic Stimulation of α1-Adrenoreceptors Induces Protein Kinase C-Dependent Persistent Changes in Motoneuronal Excitability

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-HT 2 receptors. In vivo respiratory long-term facilitation (LTF) is characterized by...

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Bibliographic Details
Published in:The Journal of neuroscience 2007-04, Vol.27 (16), p.4435-4442
Main Authors: Neverova, Natalia V., Saywell, Shane A., Nashold, Lisa J., Mitchell, Gordon S., Feldman, Jack L.
Format: Article
Language:English
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Summary: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-HT 2 receptors. In vivo respiratory long-term facilitation (LTF) is characterized by a persistent 5-HT 2 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 α1-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 α1-adrenergic receptor dependent. We suggest that, in vivo , concurrent episodic activation of 5-HT 2 and α1-adrenergic receptors is necessary to produce long-lasting changes in the excitability of respiratory motoneurons, possibly involving PKC activation via the Gα 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.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.2803-06.2007