Glutamate dysregulation in the trigeminal ganglion: A novel mechanism for peripheral sensitization of the craniofacial region

Highlights • Glutamate is released from trigeminal SGCs through EAATs. • Elevated glutamate in TG excites ganglion neurons through NMDA receptors. • Blocking glutamate uptake in the TG increases neuronal discharge. • Mechanical sensitization of muscle nociceptors is induced by elevated glutamate in...

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Bibliographic Details
Published in:Neuroscience 2014-01, Vol.256, p.23-35
Main Authors: Laursen, J.C, Cairns, B.E, Dong, X.D, Kumar, U, Somvanshi, R.K, Arendt-Nielsen, L, Gazerani, P
Format: Article
Language:English
Subjects:
2-Amino-5-phosphonovalerate - pharmacology
Action Potentials - drug effects
Anesthetics, Local - pharmacology
Animals
Aspartic Acid - analogs & derivatives
Aspartic Acid - pharmacology
Biological and medical sciences
Excitatory Amino Acid Antagonists - pharmacology
Fundamental and applied biological sciences. Psychology
Glutamic Acid - metabolism
Glutamic Acid - pharmacology
In Vitro Techniques
Lidocaine - pharmacology
Male
Mice
Muscle, Skeletal - innervation
Neural Conduction - drug effects
Neurology
Neurons - drug effects
Neurons - physiology
Potassium Chloride - pharmacology
Rats
Rats, Sprague-Dawley
Sensory Thresholds - drug effects
Sensory Thresholds - physiology
Time Factors
Trigeminal Ganglion - metabolism
Vertebrates: nervous system and sense organs
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Summary:Highlights • Glutamate is released from trigeminal SGCs through EAATs. • Elevated glutamate in TG excites ganglion neurons through NMDA receptors. • Blocking glutamate uptake in the TG increases neuronal discharge. • Mechanical sensitization of muscle nociceptors is induced by elevated glutamate in the TG. • Mechanical sensitization is due to a peripheral mechanism.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2013.10.009