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

GluN2B N-methyl-D-aspartate receptor and excitatory amino acid transporter 3 are upregulated in primary sensory neurons after 7 days of morphine administration in rats

“…Recent studies indicate that glutamatergic transmission occurs in sensory ganglions and that intraganglionic glutamate receptors are involved in certain forms of pain such as neuropathic pain [22; 42; 44]. We therefore investigated glutamate receptor responses in primary sensory neurons of rats after OIH was induced by sustained morphine administration for 7 days.…”

“…Peripheral NMDARs, however, might also have been involved and could constitute better therapeutic targets because of the fewer side effects of NMDAR antagonists that do not cross the blood-brain-barrier [57]. For this reason, we chose to study OIH associated changes in the DRG since in this peripheral location opiate and glutamate receptors are abundant and participate in nociceptive transmission [21; 22; 36; 42; 44]. We investigated changes in glutamate receptors and transporters expressed on the neurons of the lumbar DRGs of rats that were administered morphine for 7 days and showed clear signs of OIH.…”

Association between salt substitutes/enhancers and changes in sodium levels in fast-food restaurants: a cross-sectional analysis

“…50 Glutamate is the most ubiquitous excitatory neurotransmitter in the body, 51 and it has been demonstrated to play a critical role in headache pathophysiology in animal models and human studies. 21,22,46,[52][53][54][55][56][57] Previous studies have detected a dose-response relationship when MSG is administered at increasing levels. [23][24][25] One study suggested that the threshold for reactivity may be 2.5 g 23 and anecdotally reported that a highly seasoned restaurant meal could provide as much as 5 g of MSG.…”

Influence of pro-algesic foods on chronic pain conditions

“…Inhibition of glutamate reuptake by a caffeine mediated block, could lead to elevated levels of glutamate. EAAT1-3 have been found to be expressed by trigeminal ganglion neurons and their associated satellite glial cells (Figure2) [68]. Indeed, inhibition of glutamate reuptake in the trigeminal ganglion leads to increased firing and mechanical sensitization of temporalis muscle nociceptors (Figure 3) [68].…”

“…EAAT1-3 have been found to be expressed by trigeminal ganglion neurons and their associated satellite glial cells (Figure2) [68]. Indeed, inhibition of glutamate reuptake in the trigeminal ganglion leads to increased firing and mechanical sensitization of temporalis muscle nociceptors (Figure 3) [68]. As pain in the temporalis muscle is associated with headaches, the ability of caffeine to inhibit EAAT3 may also contribute to altered pain sensitivity and headache.…”