Local group I mGluR antagonists reduce TMJ-evoked activity of trigeminal subnucleus caudalis neurons in female rats

Tashiro, Akimasa; Nishida, Yasuhiro; Bereiter, David A.

doi:10.1016/j.neuroscience.2015.04.051

Cited by 5 publications

(7 citation statements)

References 76 publications

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“…In addition, the mGluR1 may be involved in the establishment of central sensitization [102]. These two observations demonstrate the functional influence of mGluR1 on central structures modulating and processing trigeminally mediated pain signals [97]. Interestingly, this connection may be influenced by estrogens [97].…”

Section: Group I Mglurmentioning

confidence: 88%

“…These two observations demonstrate the functional influence of mGluR1 on central structures modulating and processing trigeminally mediated pain signals [97]. Interestingly, this connection may be influenced by estrogens [97]. In contrast to the mGluR5, the mGluR1 is much less expressed in the TCC compared to the other central areas, in particular, the thalamus [105].…”

Section: Group I Mglurmentioning

confidence: 92%

“…Within the CNS, the receptor has been identified in the TCC as well as in the thalamus, hypothalamus, and in inhibitory structures belonging to the descending modulating network such as the periaqueductal gray [105]. As observed in mGluR5 receptors, stimulation of mGluR1 receptors on peripheral nociceptive trigeminal neurons induces a facilitation within the TCC [97]. In addition, the mGluR1 may be involved in the establishment of central sensitization [102].…”

Section: Group I Mglurmentioning

confidence: 99%

“…In relationship to migraine and trigeminal pain, mGluRs belonging to group I, in particular mGluR5, are the most investigated. The mGluR5 are located in trigeminal sensory afferents [93,94], the trigeminal ganglion [95], and in the TCC [96][97][98][99]. From a functional perspective, the receptor has been shown to be involved in several types of pain including inflammatory and neuropathic pain [100,101].…”

Section: Group I Mglurmentioning

confidence: 99%

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Glutamate and Its Receptors as Therapeutic Targets for Migraine

2018

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There is substantial evidence indicating a role for glutamate in migraine. Levels of glutamate are higher in the brain and possibly also in the peripheral circulation in migraine patients, particularly during attacks. Altered blood levels of kynurenines, endogenous modulators of glutamate receptors, have been reported in migraine patients. Population genetic studies implicate genes that are involved with glutamate signaling in migraine, and gene mutations responsible for familial hemiplegic migraine and other familial migraine syndromes may influence glutamate signaling. Animal studies indicate that glutamate plays a key role in pain transmission, central sensitization, and cortical spreading depression. Multiple therapies that target glutamate receptors including magnesium, topiramate, memantine, and ketamine have been reported to have efficacy in the treatment of migraine, although with the exception of topiramate, the evidence for the efficacy of these therapies is not strong. Also, because all of these therapies have other mechanisms of action, it is not possible to conclude that the efficacy of these drugs is entirely due to their effects on glutamate receptors. Further studies are needed to more clearly delineate the possible roles of glutamate and its specific receptor subtypes in migraine and to identify new ways of targeting glutamate for migraine therapy.

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Section: Group I Mglurmentioning

confidence: 88%

Section: Group I Mglurmentioning

confidence: 92%

Section: Group I Mglurmentioning

confidence: 99%

Section: Group I Mglurmentioning

confidence: 99%

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Glutamate and Its Receptors as Therapeutic Targets for Migraine

2018

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“…The superficial laminae at the Vc/C1‐2 region of the trigeminal nucleus caudalis was treated topically with either an mGluR1 antagnoist 7‐hydroxyimino‐cyclopropa‐chromen‐1a‐carboxylateethyl ester (CPCCOEt) or MGluR5 receptor antagonist 2‐methyl‐6‐phenylethynyl‐pyridine (MPEP) and the TMJ was injected with ATP to evoke neural activity. When the high estrogen group was compared to the low estrogen rats, unit activity was reduced along with firing response duration, but the relationship was not prominent enough to conclude that MGluRs are modulated by estrogen status (Tashiro et al, ). However, it should be noted that their high dose was pharmacologic as proestrus in normally 60–70 pg/ml and proestrus lasts no more than 1 day in normal intact rats (Butcher et al, ; Kramer & Bellinger, ).…”

Section: Pharmacologic Administration Of Estrogen Leads To Varied Resmentioning

confidence: 99%

Estrogenic effects on temporomandibular disorder and pain

Stinson¹,

Bellinger²,

Puri³

et al. 2019

J Appl Biobehavioral Res

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Purpose It has become more apparent that studies focusing on the effect of sex steroids on orofacial pain in humans and animals require careful attention to the methods of hormone replacement. As a result, the purpose of this review is to highlight differences in estrogen concentration and its effects on temporomandibular joint (TMJ) pain and behavior. Methods This literature review searched keywords TMJ, orofacial, pain, nociception sex steroids, estrous cycle, menstrual cycle estradiol, and progesterone. Results In the case of estrogen, the change in concentration was a consideration, as a rise in estrogen can lead to protective effects and a decrease in estrogen appears to exacerbate the pain response. The dosage and timing was important when administering sex steroids as many orofacial pain studies conducted on animals have used large pharmacologic dosages and/or have given the hormone in a nonphysiologic way that does not mimic natural secretion patterns. Conclusions The results demonstrate that when performing studies or experiments these factors can result in alteration of the pain or behavioral response, as well as, joint structure and inflammatory response. Therefore, these factors must be considered when designing experiments focused on determining the mechanisms of action for sex steroids.

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