scholarly journals The Change of Nociceptive Neurons in the Rat Trigeminal Ganglia at Different Postnatal Ages

2017 ◽  
Vol 23 (2) ◽  
pp. 190-193 ◽  
Author(s):  
Mei-Qi Zeng ◽  
Jun-Fei Niu ◽  
Ping Luan ◽  
Ying Ying ◽  
Rui-Ping Pang ◽  
...  
Keyword(s):  
Trigeminal Ganglia ◽  
Nociceptive Neurons

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

2020 ◽  
Vol 21 (8) ◽  
pp. 2938
Author(s):  
Timea Aczél ◽  
Angéla Kecskés ◽  
József Kun ◽  
Kálmán Szenthe ◽  
Ferenc Bánáti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glial Cells ◽  
Orofacial Pain ◽  
Model Potential ◽  
Trigeminal System ◽  
Trigeminal Ganglia ◽  
Peripheral Sensitization ◽  
Satellite Glial Cells ◽  
Pain Model ◽  
Nociceptive Neurons

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.

Conditional gene deletion in primary nociceptive neurons of trigeminal ganglia and dorsal root ganglia

genesis ◽  
2004 ◽  
Vol 38 (3) ◽  
pp. 122-129 ◽  
Author(s):  
Nitin Agarwal ◽  
Stefan Offermanns ◽  
Rohini Kuner
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Gene Deletion ◽  
Trigeminal Ganglia ◽  
Nociceptive Neurons

scholarly journals Expression and function of a CP339,818-sensitive K+ current in a subpopulation of putative nociceptive neurons from adult mouse trigeminal ganglia

2015 ◽  
Vol 113 (7) ◽  
pp. 2653-2665 ◽  
Author(s):  
Luigi Sforna ◽  
Maria Cristina D'Adamo ◽  
Ilenio Servettini ◽  
Luca Guglielmi ◽  
Mauro Pessia ◽  
...  
Keyword(s):  
Steady State ◽  
Firing Frequency ◽  
Resting Potential ◽  
Trigeminal Ganglia ◽  
Nociceptive Neurons ◽  
Steady State Inactivation ◽  
Biophysical Study ◽  
K Current ◽  
Membrane Resting Potential ◽  
And Function

Trigeminal ganglion (TG) neurons are functionally and morphologically heterogeneous, and the molecular basis of this heterogeneity is still not fully understood. Here we describe experiments showing that a subpopulation of neurons expresses a delayed-rectifying K+ current ( IDRK) with a characteristically high (nanomolar) sensitivity to the dihydroquinoline CP339,818 (CP). Although submicromolar CP has previously been shown to selectively block Kv1.3 and Kv1.4 channels, the CP-sensitive IDRK found in TG neurons could not be associated with either of these two K+ channels. It could neither be associated with Kv2.1 channels homomeric or heteromerically associated with the Kv9.2, Kv9.3, or Kv6.4 subunits, whose block by CP, tested using two-electrode voltage-clamp recordings from Xenopus oocytes, resulted in the low micromolar range, nor to the Kv7 subfamily, given the lack of blocking efficacy of 3 μM XE991. Within the group of multiple-firing neurons considered in this study, the CP-sensitive IDRK was preferentially expressed in a subpopulation showing several nociceptive markers, such as small membrane capacitance, sensitivity to capsaicin, and slow afterhyperpolarization (AHP); in these neurons the CP-sensitive IDRK controls the membrane resting potential, the firing frequency, and the AHP duration. A biophysical study of the CP-sensitive IDRK indicated the presence of two kinetically distinct components: a fast deactivating component having a relatively depolarized steady-state inactivation ( IDRKf) and a slow deactivating component with a more hyperpolarized V1/2 for steady-state inactivation ( IDRKs).

C mechanical nociceptive neurons in the crotaline trigeminal ganglia

1994 ◽  
Vol 179 (1-2) ◽  
pp. 33-36 ◽  
Author(s):  
Shin-ichi Terashima ◽  
Yun-Fei Liang
Keyword(s):  
Trigeminal Ganglia ◽  
Nociceptive Neurons

scholarly journals Loss of Elp1 disrupts trigeminal ganglion neurodevelopment in a model of Familial Dysautonomia

2021 ◽  
Author(s):  
Carrie E Leonard ◽  
Frances Lefcort ◽  
Lisa A Taneyhill
Keyword(s):  
Neural Crest ◽  
Trigeminal Ganglion ◽  
Facial Pain ◽  
Familial Dysautonomia ◽  
Trigeminal Ganglia ◽  
Nociceptive Neurons ◽  
Target Innervation ◽  
Trigeminal Neurons ◽  
Complex Protein ◽  
Trigeminal Nerves

Familial Dysautonomia (FD) is a sensory and autonomic neuropathy caused by a mutation in Elongator complex protein 1 (ELP1). FD patients have small trigeminal nerves and impaired perception of facial pain and temperature. These signals are relayed by nociceptive neurons in the trigeminal ganglion, a structure comprised of both neural crest- and placode-derived cells. Mice lacking Elp1 in neural crest derivatives (Elp1 CKO) are born with smaller trigeminal ganglia, suggesting Elp1 is important for trigeminal ganglion development, yet the function of Elp1 in this context is unknown. We demonstrate Elp1 expression in both neural crest- and placode-derived trigeminal neurons, which our data suggest give rise to primarily TrkA- and TrkB/C-expressing neurons, respectively. While Elp1 is not required for initial trigeminal ganglion formation, Elp1 CKO trigeminal neurons exhibit abnormal axon outgrowth and decreased target innervation. Developing nociceptors that express the receptor TrkA are especially vulnerable to Elp1 loss. TrkA expression is decreased in Elp1 CKO trigeminal nerve endings, coinciding with increased cell death. Subsequently, fewer TrkA neurons are present in the Elp1 CKO trigeminal ganglion, indicating Elp1 supports the target innervation and survival of trigeminal nociceptors. These findings explain the loss of facial pain and temperature sensation in FD.

Effects of Oestrogen on Trigeminal Ganglia in Culture: Implications for Hormonal Effects on Migraine

Cephalalgia ◽  
2006 ◽  
Vol 26 (1) ◽  
pp. 33-42 ◽  
Author(s):  
V Puri ◽  
S Puri ◽  
SR Svojanovsky ◽  
S Mathur ◽  
RR Macgregor ◽  
...  
Keyword(s):  
Zinc Finger Protein ◽  
Early Gene ◽  
Trigeminal Ganglia ◽  
Female Rat ◽  
Protein Activity ◽  
Trigeminovascular System ◽  
Oestrogen Treatment ◽  
Nociceptive Neurons ◽  
Phosphoserine Aminotransferase

Although migraine is more common in women than men and often linked to the menstrual cycle, few studies have investigated the biological basis of hormonal influences on the trigeminovascular system. In the present study we investigated the effect of physiological levels (10-9 M) oestrogen on female rat trigeminal ganglia in vitro. Immunocytochemical analysis demonstrated the presence of oestrogen receptor-alpha in a predominantly cytoplasmic location and in neurites. Microarray analysis demonstrated that oestrogen treatment regulates several genes with potential relevance to menstrual migraine. The genes that were upregulated included synapsin-2, endothelin receptor type B, activity and neurotransmitter-induced early gene 7 (ania-7), phosphoserine aminotransferase, MHC-1b, and ERK-1. Down-regulated genes included IL-R1, bradykinin B2 receptor, N- tropomodulin, CCL20, GABA transporter protein, fetal intestinal lactase-phlorizin hydrolase, carcinoembryonic antigen-related protein, zinc finger protein 36, epsin 1 and cysteine string protein. Protein activity assays demonstrated that exposure of the cultured neurons to oestrogen leads to activation of ERK, which has been linked to inflammatory pain. Immunocytochemistry demonstrated that activated ERK was present in neurons containing peripherin, a marker of nociceptive neurons. Several of the genes in the present study may provide potential targets for understanding the association of oestrogen with migraine and other hormone- related orofacial pain.

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