Iontophoretic analysis of the pharmacologic mechanisms responsible for initiation and modulation of trigeminal motoneuronal discharge evoked by intra-oral afferent stimulation

Katakura, Nobuo; Chandler, Scott H.

doi:10.1016/0006-8993(91)90600-z

Cited by 26 publications

(19 citation statements)

References 36 publications

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“…In contrast, monosynaptic EPSP to jaw-closer motoneurons elicited from spindle or periodontal receptor fibers in mesencephalic nucleus of V, when examined intracellularly (1273) rather than extracellularly (206,656), show a small but significant NMDA component. The greater sensitivity to NMDA antagonists of extracellular potentials induced in trigeminal motoneurons through stimulation of tooth pulp versus oral mucosa further supports the differential involvement of NMDA and non-NMDA receptors (609). Similarly, the NMDA contribution to dual component EPSP elicited from the NTS fiber tract onto ambigual motoneurons in medullary slices, believed to be the efferent limb of the swallowing reflex, is larger than seen at most other cranial motoneuron synapses (1336).…”

Section: Ii) Cranial Reflex Transmissionmentioning

confidence: 86%

“…In contrast, all recent work indicates that the predominant postsynaptic effects of NE are excitatory, suggesting that the initial findings resulted from a methodological artifact (1362). Thus, in cranial and spinal motoneurons, NE causes a slow membrane depolarization associated with a decrease in input conductance (332,701,958,1303,1360) and enhances firing responses to glutamatergic inputs, whether applied exogenously or released endogenously (395, 608,609,[1360][1361][1362]. These effects of NE are postsynaptic, since they are preserved in the presence of TTX or a high-Mg 2+ , low-Ca 2+ synaptic blockade medium.…”

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

“…An α 1 -adrenoceptor is involved since effects of NE are 1) blocked by α-adrenoceptor antagonists, prazosin and phentolamine, but not by the β-adrenoceptor antagonists propranolol or sotalol, and 2) mimicked by the α 1 -adrenoceptor agonist phenylephrine but not by either the α 2 -adrenoceptor agonist UK-14,304 or the β-adrenoceptor agonist isoproterenol (332,608,609,958,1323). On the basis of relative agonist/antagonist potencies and insensitivity of the response to chloroethylclonidine, the facilitation of spinal motoneuronal activity by NE may be mediated primarily by the α 1A -adrenoceptor subtype (1323).…”

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

“…For example, muscle EMG activity and the flexor response to afferent nerve volleys in spinal rats are inhibited by the α 2 -adrenoceptor agonist clonidine (1074,1265); in a subpopulation of trigeminal motoneurons, clonidine suppresses motoneuronal discharge induced by oral stimulation, an effect blocked by the α 2 -antagonist yohimbine (609). This effect of α 2 -adrenoceptor activation could be mediated by direct actions on premotor interneurons, or by pre-or postsynaptic actions at the level of the motoneurons.…”

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

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Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

537

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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Section: Ii) Cranial Reflex Transmissionmentioning

confidence: 86%

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

Section: Pre-and Postsynaptic Actions Of Ne On Motoneurons-early Workmentioning

confidence: 99%

See 2 more Smart Citations

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

537

482

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“…However, considerable evidence supports ␣ 2 -receptor-mediated inhibition of motoneuron output. For example, ␣ 2 -receptor mechanisms contribute to the long-term depression of phrenic and XII output induced by episodic hypercapnia (3) and suppress the responses of trigeminal motoneurons to oral stimulation (29). In addition, clonidine inhibits EMG activity and the flexor responses of spinal rats to afferent nerve volleys (65).…”

Section: Discussionmentioning

confidence: 99%

Noradrenergic modulation of XII motoneuron inspiratory activity does not involve α₂-receptor inhibition of theI_hcurrent or presynaptic glutamate release

Adachi¹,

Robinson²,

Miles³

et al. 2005

Journal of Applied Physiology

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. Noradrenergic modulation of XII motoneuron inspiratory activity does not involve ␣ 2-receptor inhibition of the Ih current or presynaptic glutamate release. J Appl Physiol 98: 1297 -1308 ,2005 .FirstpublishedDecember3,2004doi:10.1152/japplphysiol. 00977.2004.-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 Ϯ 3% of control but had no effect on inspiratory synaptic currents. It also reduced the I h current by ϳ40%, but an Ih current blocker (ZD7288), at concentrations that blocked ϳ80% of Ih, had no effect on inspiratory burst amplitude. The clonidine inhibition was unaffected by the GABAA antagonist (ϩ)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) Ih 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 HYPOGLOSSAL (XII) motoneurons contribute to a number of rhythmic motor behaviors that are functional from the time of birth including swallowing, coughing, chewing, and vocalization (4, 53). They also play an important role in breathing whereby they help to maintain upper airway patency during inspiration by increasing genioglossus muscle tone. Their critical role in maintaining airway patency and the fact that airway dysfunction during sleep is implicated in obstructive sleep apnea and some cases of sudden infant death syndrome, combined with their utility for examining basic questions of signal processing, underlie the intense interest in understanding the neuromodulatory control of XII motoneuron excitability (18,45,52,55,62).Noradrenergic signaling cascades, for...

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NMDA receptor NR1 and NR2A/B subunit expression in trigeminal neurons during early postnatal development

Turman¹,

Ajdari²,

Chandler³

1999

J. Comp. Neurol.

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Trigeminal motoneurons (Mo5), mesencephalic trigeminal neurons (Me5), and supratrigeminal (Su5) and intertrigeminal (I5) neurons are important constituents of the neural circuitry responsible for jaw movements observed during ingestive behaviors. In addition, in adult animals, N‐methyl‐D‐aspartate (NMDA) receptors are a critical component of the brainstem circuitry responsible for reflex‐ and centrally activated jaw movements. However, little is known about the expression of this receptor in circuitry used to produce neonatal jaw movements. Receptor immunohistochemistry was used to describe changes in the expression of NMDA NR1 and NR2A/B receptor subunits in Mo5, Me5, Su5, and I5 neurons during postnatal development. Rats at postnatal days (P) 1, 3, 8, 15–16, 21–24, and 28–35 were used. An affinity‐purified polyclonal antibody against the NR1 subunit and an affinity‐purified polyclonal antibody that recognizes both NR2A and 2B subunits were used to depict the expression of these subunits. In Mo5, immunoreactivity was noted for both antibodies throughout the time frame sampled. NR1 expression in Me5 neurons emerged at P1. NR2A/B expression emerged at P3 in caudal and middle regions of Me5 and at P8 for rostral regions of the nucleus. NR1 immunoreactivity was present at P1 for neurons in I5 and at P3 for neurons in the Su5 region. NR2A/B subunit expression in Su5 and I5 neurons emerged at P8. These results provide evidence for NMDA receptor subunits in neonatal trigeminal neurons used in oral–motor circuitry and suggest a role for the NMDA receptor in synaptogenesis associated with these neurons during postnatal development. J. Comp. Neurol. 409:237–249, 1999. © 1999 Wiley‐Liss, Inc.

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Iontophoretic analysis of the pharmacologic mechanisms responsible for initiation and modulation of trigeminal motoneuronal discharge evoked by intra-oral afferent stimulation

Cited by 26 publications

References 36 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

Noradrenergic modulation of XII motoneuron inspiratory activity does not involve α₂-receptor inhibition of theI_hcurrent or presynaptic glutamate release

NMDA receptor NR1 and NR2A/B subunit expression in trigeminal neurons during early postnatal development

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Iontophoretic analysis of the pharmacologic mechanisms responsible for initiation and modulation of trigeminal motoneuronal discharge evoked by intra-oral afferent stimulation

Cited by 26 publications

References 36 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

Noradrenergic modulation of XII motoneuron inspiratory activity does not involve α2-receptor inhibition of theIhcurrent or presynaptic glutamate release

NMDA receptor NR1 and NR2A/B subunit expression in trigeminal neurons during early postnatal development

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Noradrenergic modulation of XII motoneuron inspiratory activity does not involve α₂-receptor inhibition of theI_hcurrent or presynaptic glutamate release