Involvement of NMDA receptors in Zif/268 expression in the trigeminal nucleus caudalis following formalin injection into the rat whisker pad

Otahara, Noriko; Ikeda, Tetsuya; Sakoda, Sumio; Shiba, Ryosuke; Nishimori, Toshikazu

doi:10.1016/j.brainresbull.2003.08.008

Cited by 14 publications

(8 citation statements)

References 35 publications

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“…These data suggest a difference in specialization of Sp5O and Sp5C in processing nociceptive messages, Sp5O being preferentially involved in transient oral/perioral nociception, whereas Sp5C may be the only trigeminal structure specialized in sustained nociception (Duale et al, 1996). Other authors have reported neuronal activation only in Sp5C after FORM perioral stimulation, and not in other subnuclei (Nagamatsu et al, 2001; Otahara et al, 2003). In other rat studies, Pajot et al (2000) underscored the primary role of Sp5C compared with Sp5O in nociceptive transmission, suggesting species‐specific subnuclear involvement.…”

Section: Discussionmentioning

confidence: 86%

Peripheral purinergic receptor modulation influences the trigeminal ganglia nitroxidergic system in an experimental murine model of inflammatory orofacial pain

Borsani

Albertini

Labanca

et al. 2010

J of Neuroscience Research

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ATP plays an important role as an endogenous pain mediator generating and/or modulating pain signaling from the periphery to the central nervous system. The aim of this study was to analyze the role of peripheral purinergic receptors in modulation of the nitroxidergic system at a trigeminal ganglia level by monitoring changes in nitric oxide synthase isoforms. We also evaluated Fos-positive neurons in brainstem (spinal trigeminal nucleus) and pain-related behavior. We found that local administration of the P2 purinergic receptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) decreased face-rubbing activity, nitric oxide synthase isoform expression in trigeminal ganglia, and Fos expression in spinal trigeminal nucleus after subcutaneous injection of formalin. These results suggest a role for peripheral P2 purinergic receptors in orofacial pain transmission through modulation of the nitroxidergic system. .

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Section: Discussionmentioning

confidence: 86%

Peripheral purinergic receptor modulation influences the trigeminal ganglia nitroxidergic system in an experimental murine model of inflammatory orofacial pain

Borsani

Albertini

Labanca

et al. 2010

J of Neuroscience Research

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“…MK-801 (i.p., i.v.) reduces Fos-ir in the rat and cat caudal spinal trigeminal nuclei following experimental tooth (molar) movement, formalin injection in whisker pad, MO injection in TMJ, and electrical stimulation of the superior sagittal sinus (Bereiter & Bereiter, 2000; Classey et al, 2001; Otahara et al, 2003; Hattori et al, 2004). Increases in Fos-ir by carrageenan or formalin injection in the rat hindpaw can be diminished i.v.…”

Section: Peripheral Effects Of Glutamate: Biophysicalmentioning

confidence: 99%

Glutamate pharmacology and metabolism in peripheral primary afferents: Physiological and pathophysiological mechanisms

Miller

Hoffman

Sutharshan

et al. 2011

Pharmacology & Therapeutics

121

129

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In addition to using glutamate as a neurotransmitter at central synapses, many primary sensory neurons release glutamate from peripheral terminals. Primary sensory neurons with cell bodies in dorsal root or trigeminal ganglia produce glutaminase, the synthetic enzyme for glutamate, and transport the enzyme in mitochondria to peripheral terminals. Vesicular glutamate transporters fill neurotransmitter vesicles with glutamate and they are shipped to peripheral terminals. Intense noxious stimuli or tissue damage causes glutamate to be released from peripheral afferent nerve terminals and augmented release occurs during acute and chronic inflammation. The site of action for glutamate can be at the autologous or nearby nerve terminals. Peripheral nerve terminals contain both ionotropic and metabotropic excitatory amino acid receptors (EAARs) and activation of these receptors can lower the activation threshold and increase the excitability of primary afferents. Antagonism of EAARs can reduce excitability of activated afferents and produce antinociception in many animal models of acute and chronic pain. Glutamate injected into human skin and muscle causes acute pain. Trauma in humans, such as arthritis, myalgia, and tendonitis, elevates glutamate levels in affected tissues. There is evidence that EAAR antagonism at peripheral sites can provide relief in some chronic pain sufferers.

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“…NMDA receptor antagonists including the high‐affinity channel blocker MK‐801 block trigeminal nociceptive transmission (Storer & Goadsby, ). The obligate NR1 subunit of NMDA receptors exists in the trigeminal nucleus caudalis (Bereiter & Bereiter, ; Otahara, Ikeda, Sakoda, Shiba, & Nishimori, ) so NMDA channel agonists and blockers may act to modulate nociceptive neurotransmission at the second‐order synapse in this region. We therefore investigated the efficacy of Mg 2+ and memantine to modulate trigeminovascular nociception in our rat model of trigeminovascular nociceptive activation, comparing direct application onto receptors in the trigeminal nucleus caudalis via microiontophoresis with systemic administration.…”

Section: Introductionmentioning

confidence: 99%

N‐Methyl‐d‐aspartate receptor open‐channel blockers memantine and magnesium modulate nociceptive trigeminovascular neurotransmission in rats

Hoffmann

Storer

Park

et al. 2019

Eur J of Neuroscience

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Experimental and clinical studies suggest that the low‐affinity N‐methyl‐d‐aspartate (NMDA) receptor open‐channel blockers Mg2+ and memantine are effective in reducing trigeminal nociceptive activation. The aim of this study was to investigate the apparent effectiveness of these channel blockers using a model of trigeminal activation in vivo. Rats were anaesthetized before electrically stimulating the dura mater adjacent the middle meningeal artery. Neurons responding to stimulation were recorded extracellularly using electrophysiological methods. l‐Glutamate or NMDA, and Mg2+, memantine, or sodium controls were applied locally using microiontophoresis. Microiontophoretic application of Mg2+ or memantine into the trigeminocervical complex inhibited mechanically and electrically stimulated craniovascular afferents, and l‐glutamate or NMDA‐evoked neuronal activity at the second‐order trigeminal synapse of craniovascular afferents. By contrast, intravenous administration of MgSO4 (100 mg/kg) or memantine (10 mg/kg) did not significantly affect electrically stimulated afferent‐evoked activity within the trigeminocervical complex. The Mg2+ and memantine concentrations achieved after systemic administration may not effectively inhibit activation of the trigeminocervical complex, perhaps providing an explanation for the relatively poor efficacy of these NMDA receptor open‐channel blockers for headache treatment in clinical studies. Nevertheless, the present results suggest blocking of NMDA‐receptor open channels inhibits nociceptive activation of the trigeminocervical complex. Further exploration of such channel blockers as a therapeutic strategy for primary head pain is warranted.

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Involvement of NMDA receptors in Zif/268 expression in the trigeminal nucleus caudalis following formalin injection into the rat whisker pad

Cited by 14 publications

References 35 publications

Peripheral purinergic receptor modulation influences the trigeminal ganglia nitroxidergic system in an experimental murine model of inflammatory orofacial pain

Peripheral purinergic receptor modulation influences the trigeminal ganglia nitroxidergic system in an experimental murine model of inflammatory orofacial pain

Glutamate pharmacology and metabolism in peripheral primary afferents: Physiological and pathophysiological mechanisms

N‐Methyl‐d‐aspartate receptor open‐channel blockers memantine and magnesium modulate nociceptive trigeminovascular neurotransmission in rats

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