title: Evidence for glutamate as a neuroglial transmitter within sensory ganglia.
abstract: This study examines key elements of glutamatergic transmission within sensory ganglia of the rat. We show that the soma of primary sensory neurons release glutamate when depolarized. Using acute dissociated mixed neuronal/glia cultures of dorsal root ganglia (DRG) or trigeminal ganglia and a colorimetric assay, we show that when glutamate uptake by satellite glial cells (SGCs) is inhibited, KCl stimulation leads to simultaneous increase of glutamate in the culture medium. With calcium imaging we see that the soma of primary sensory neurons and SGCs respond to AMPA, NMDA, kainate and mGluR agonists, and selective antagonists block this response. Using whole cell patch-clamp technique, inward currents were recorded from small diameter (<30 µm) DRG neurons from intact DRGs (ex-vivo whole ganglion preparation) in response to local application of the above glutamate receptor agonists. Following a chronic constriction injury (CCI) of either the inferior orbital nerve or the sciatic nerve, glutamate expression increases in the trigeminal ganglia and DRG respectively. This increase occurs in neurons of all diameters and is present in the somata of neurons with injured axons as well as in somata of neighboring uninjured neurons. These data provides additional evidence that glutamate can be released within the sensory ganglion, and that the somata of primary sensory neurons as well as SGCs express functional glutamate receptors at their surface. These findings, together with our previous gene knockdown data, suggest that glutamatergic transmission within the ganglion could impact nociceptive threshold.
authors.affiliation: Department of Anatomy, University of California San Francisco, San Francisco, California, United States of America.
authors.forename: Ling-Hsuan
authors.initials: LH
authors.lastname: Kung
authors.forename: Kerui
authors.initials: K
authors.lastname: Gong
authors.forename: Mary
authors.initials: M
authors.lastname: Adedoyin
authors.forename: Johnson
authors.initials: J
authors.lastname: Ng
authors.forename: Aditi
authors.initials: A
authors.lastname: Bhargava
authors.forename: Peter T
authors.initials: PT
authors.lastname: Ohara
authors.forename: Luc
authors.initials: L
authors.lastname: Jasmin
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D017077:Culture Media, Conditioned / Q000378:metabolism; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D017950:Ganglia, Sensory / Q000166:cytology / Q000378:metabolism*; D005727:Ganglia, Spinal / Q000166:cytology / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D018613:Microscopy, Confocal; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D018377:Neurotransmitter Agents / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017470:Receptors, Glutamate / Q000378:metabolism; D027161:Satellite Cells, Perineuronal / Q000378:metabolism; D012584:Sciatic Nerve / Q000378:metabolism / Q000601:surgery; D012668:Trigeminal Ganglion / Q000166:cytology / Q000378:metabolism
chemical_list: D017077:Culture Media, Conditioned; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018377:Neurotransmitter Agents; D017470:Receptors, Glutamate; D018698:Glutamic Acid; D002118:Calcium