Distribution of hemokinin-1 in the rat trigeminal ganglion and trigeminal sensory nuclear complex

Igawa, Kaori; Funahashi, Hideki; Miyahara, Yu; Naono-Nakayama, Rumi; Matsuo, Hitoshi; Yamashita, Yuichi; Sakoda, Sumio; Nishimori, Toshikazu; Ishida, Yoshiteru

doi:10.1016/j.archoralbio.2017.03.004

Cited by 5 publications

(6 citation statements)

References 34 publications

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“…In the present study, we confirmed the presence of Tac4 mRNA in the TG and established its upregulation in response to orofacial inflammation. While it had been previously shown that HK-1 was expressed widely in the nervous system including the brain, spinal cord, dorsal root ganglia, brain stem and the TG [34,39], this is the first study to assess the changes of Tac4 expression alterations under pathological conditions. HK-1 had only been detected in small and medium-size neurons by immunohistochemistry in the rat TG [39], but in the present study, we showed that besides the neuronal expression, Tac4 mRNA was also expressed in satellite glial cells of the TG.…”

Section: Discussionmentioning

confidence: 98%

“…Since the structures of HK-1 and SP are very similar, it is difficult to proceed with peptide detection, localization and measurement. Although a few studies reported antibody development (e.g., [38]) or a recent immunohistochemical study on the TG with an in-house developed antibody [39], there are still no commercially available antibodies against HK-1. Despite the structural similarities and common receptors of HK-1 and SP, some of their functions appear to be different, even opposing each other [36,[40][41][42][43].…”

Section: Introductionmentioning

confidence: 99%

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Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

Aczél

Kecskés

Kun

et al. 2020

IJMS

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A large percentage of primary sensory neurons in the trigeminal ganglia (TG) contain neuropeptides such as tachykinins or calcitonin gene-related peptide. Neuropeptides released from the central terminals of primary afferents sensitize the secondary nociceptive neurons in the trigeminal nucleus caudalis (TNC), but also activate glial cells contributing to neuroinflammation and consequent sensitization in chronic orofacial pain and migraine. In the present study, we investigated the newest member of the tachykinin family, hemokinin-1 (HK-1) encoded by the Tac4 gene in the trigeminal system. HK-1 had been shown to participate in inflammation and hyperalgesia in various models, but its role has not been investigated in orofacial pain or headache. In the complete Freund’s adjuvant (CFA)-induced inflammatory orofacial pain model, we showed that Tac4 expression increased in the TG in response to inflammation. Duration-dependent Tac4 upregulation was associated with the extent of the facial allodynia. Tac4 was detected in both TG neurons and satellite glial cells (SGC) by the ultrasensitive RNAscope in situ hybridization. We also compared gene expression changes of selected neuronal and glial sensitization and neuroinflammation markers between wild-type and Tac4-deficient (Tac4-/-) mice. Expression of the SGC/astrocyte marker in the TG and TNC was significantly lower in intact and saline/CFA-treated Tac4-/- mice. The procedural stress-related increase of the SGC/astrocyte marker was also strongly attenuated in Tac4-/- mice. Analysis of TG samples with a mouse neuroinflammation panel of 770 genes revealed that regulation of microglia and cytotoxic cell-related genes were significantly different in saline-treated Tac4-/- mice compared to their wild-types. It is concluded that HK-1 may participate in neuron-glia interactions both under physiological and inflammatory conditions and mediate pain in the trigeminal system.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

Aczél

Kecskés

Kun

et al. 2020

IJMS

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“…Large amounts of SP can directly induce sensory neuron excitability, which leads to hyperalgesia 43 . SP, which is the main messenger of harmful information, can be synthesized by TG cells and delivered to the trigeminal sensory nucleus and the peripheral head and face through central and peripheral synapses, respectively 45,46 . Studies have reported that after nerve injury, SCs synthesize and release NGF, which can promote SP synthesis 47 .…”

Section: Scs and Production Of Tnmentioning

confidence: 99%

“…43 SP, which is the main messenger of harmful information, can be synthesized by TG cells and delivered to the trigeminal sensory nucleus and the peripheral head and face through central and peripheral synapses, respectively. 45,46 Studies have reported that after nerve injury, SCs synthesize and release NGF, which can promote SP synthesis. 47 Moreover, treatment with SP receptor blockers can alleviate TN caused by infraorbital nerve injury.…”

Section: Scs and Production Of Tnmentioning

confidence: 99%

Schwann cells and trigeminal neuralgia

et al. 2020

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Schwann cells (SCs) are components of the peripheral nerve myelin sheath, which supports and nourishes axons. Upon injury of the trigeminal nerve, SCs are activated and cause trigeminal neuralgia by engulfing the myelin sheath and secreting various neurotrophic factors. Further, SCs can repair the Injury nerve, and thus alleviate trigeminal neuralgia. Here, we briefly describe the development and activation of SCs after nerve damage. Moreover, we expound on the occurrence, regulation, and treatment of trigeminal neuralgia; further, we point out the current research deficiencies and future research directions.

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“…8 SP can be synthesized and released from primary afferent neurons in TG. 9 Especially in the spinal dorsal horn, SP is able to produce a persistent spontaneous pain and hyperalgesia. 10,11 Nevertheless, whether TMJ synovitis can affect SP expression in primary afferent neurons of TG remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Peripheral and central substance P expression in rat CFA-induced TMJ synovitis pain

Jiang

Feng

et al. 2019

Mol Pain

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Synovitis contributes to temporomandibular joint (TMJ) pain, nevertheless, the detailed nociceptive mechanism remains unclear. In this study, a rat model of TMJ synovitis was induced by intra-articular injection with complete Freund's adjuvant (CFA). After CFA-induced synovitis, pain behaviors were observed. Then, TMJ, trigeminal ganglion, and trigeminal nucleus caudalis (TNC) tissues were collected, and immunohistochemistry was used to detect the expression of substance P (SP) and protein gene product 9.5 (PGP9.5) in the synovium tissue. Furthermore, the gene expression level of SP and PGP9.5 in synovium was detected by reverse transcription-polymerase chain reaction (RT-PCR). Afterwards, the expression of SP in the trigeminal ganglion and TNC and c-fos in the TNC was detected by immunohistochemistry. Compared with the control group, the expression of SP and PGP9.5 nerve fibers density and gene levels of them in the synovium tissue were significantly increased in CFA-induced TMJ synovitis rats. Similarly, SP expression in the trigeminal ganglion and TNC, and c-fos expression in the TNC were also obviously increased in CFA-induced TMJ synovitis rats. Collectively, CFA-induced rat TMJ synovitis resulted in obvious pain. This nociceptive reaction could be attributed to the augmented quantity of SP and PGP9.5 positive-stained nerve fibers distributed in the inflammatory synovium as well as enhanced SP expression in the trigeminal ganglion and TNC tissue. c-fos expression in the rat TNC illustrates CFA-induced TMJ synovitis can evoke the acute pain.

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Distribution of hemokinin-1 in the rat trigeminal ganglion and trigeminal sensory nuclear complex

Cited by 5 publications

References 34 publications

Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

Hemokinin-1 Gene Expression Is Upregulated in Trigeminal Ganglia in an Inflammatory Orofacial Pain Model: Potential Role in Peripheral Sensitization

Schwann cells and trigeminal neuralgia

Peripheral and central substance P expression in rat CFA-induced TMJ synovitis pain

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