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Noradrenergic modulation of XII motoneuron inspiratory activity does not involve ₂-receptor inhibition of the I_h current or presynaptic glutamate release

Department of Physiology, Faculty of Medicine and Health Science, University of Auckland, Auckland, New Zealand

Submitted 7 September 2004 ; accepted in final form 30 November 2004

Norepinephrine has powerful and diverse modulatory effects on hypoglossal (XII) motoneuron activity, which is important in maintaining airway patency. The objective was to test two hypotheses that ₂-adrenoceptor-mediated, presynaptic inhibition of glutamatergic inspiratory drive (Selvaratnam SR, Parkis MA, and Funk GD. Brain Res 805: 104–115, 1998) and postsynaptic inhibition of the hyperpolarization-activated inward current (I_h) (Parkis MA and Berger AJ. Brain Res 769: 108–118, 1997) modulate XII inspiratory activity. Nerve and whole cell recordings were applied to rhythmic medullary slice preparations from neonatal rats (postnatal days 0–4) to monitor XII inspiratory burst amplitude and motoneuron properties. Application of an ₂-receptor agonist (clonidine, 1 mM) to the XII nucleus reduced inspiratory burst amplitude to 71 ± 3% of control but had no effect on inspiratory synaptic currents. It also reduced the I_h current by 40%, but an I_h current blocker (ZD7288), at concentrations that blocked 80% of I_h, had no effect on inspiratory burst amplitude. The clonidine inhibition was unaffected by the GABA_A antagonist (+)bicuculline but attenuated by the ₂-antagonist rauwolscine and the imidazoline 1 (I₁) antagonist efaroxan. The I₁ agonist rilmenidine, but not the ₂-agonist UK14304, inhibited XII output. Clonidine also reduced action potential amplitude or impaired repetitive firing. Although a contribution from ₂, and in particular I₁, receptors remains possible, results demonstrate that 1) noradrenergic modulation of XII inspiratory activity is unlikely to involve ₂-receptor-mediated presynaptic inhibition of glutamate release or modulation of I_h; 2) inhibition of repetitive firing is a major factor underlying the inhibition of XII output by clonidine; and 3) I_h is present in neonatal XII motoneurons but does not contribute to shaping their inspiratory activity.

airway control; ₂-adrenoceptor; hyperpolarization-activated inward current; whole cell recording; rat; clonidine

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