WordNet

the main sensory nerve of the face and motor nerve for the muscles of mastication (同)trigeminal_nerve, trigeminus, nervus_trigeminus, fifth_cranial_nerve

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1. 三叉神経痛 trigeminal neuralgia
2. 頭蓋顔面痛の概要 overview of craniofacial pain
3. 三叉神経・自律神経性頭痛の病態生理 pathophysiology of the trigeminal autonomic cephalalgias
4. 短時間持続性片側神経痛様頭痛発作：臨床的特徴および診断 short lasting unilateral neuralgiform headache attacks clinical features and diagnosis
5. 短時間持続性片側神経痛様頭痛発作：治療 short lasting unilateral neuralgiform headache attacks treatment

English Journal

Distribution of gastrin-releasing peptide in the rat trigeminal and spinal somatosensory systems.

Takanami K1, Sakamoto H, Matsuda KI, Satoh K, Tanida T, Yamada S, Inoue K, Oti T, Sakamoto T, Kawata M.Author information 1Department of Anatomy and Neurobiology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.AbstractGastrin-releasing peptide (GRP) has recently been identified as an itch-specific neuropeptide in the spinal sensory system in mice, but there are no reports of the expression and distribution of GRP in the trigeminal sensory system in mammals. We characterized and compared GRP-immunoreactive (ir) neurons in the trigeminal ganglion (TG) with those in the rat spinal dorsal root ganglion (DRG). GRP immunoreactivity was expressed in 12% of TG and 6% of DRG neurons and was restricted to the small- and medium-sized type cells. In both the TG and DRG, many GRP-ir neurons also expressed substance P and calcitonin gene-related peptide, but not isolectin B4 . The different proportions of GRP and transient receptor potential vanilloid 1 double-positive neurons in the TG and DRG imply that itch sensations via the TG and DRG pathways are transmitted through distinct mechanisms. The distribution of the axon terminals of GRP-ir primary afferents and their synaptic connectivity with the rat trigeminal sensory nuclei and spinal dorsal horn were investigated by using light and electron microscopic histochemistry. Although GRP-ir fibers were rarely observed in the trigeminal sensory nucleus principalis, oralis, and interpolaris, they were predominant in the superficial layers of the trigeminal sensory nucleus caudalis (Vc), similar to the spinal dorsal horn. Ultrastructural analysis revealed that GRP-ir terminals contained clear microvesicles and large dense-cored vesicles, and formed asymmetric synaptic contacts with a few dendrites in the Vc and spinal dorsal horn. These results suggest that GRP-dependent orofacial and spinal pruriceptive inputs are processed mainly in the superficial laminae of the Vc and spinal dorsal horn. J. Comp. Neurol. 522:1858-1873, 2014. © 2013 Wiley Periodicals, Inc.
The Journal of comparative neurology.J Comp Neurol.2014 Jun 1;522(8):1858-73. doi: 10.1002/cne.23506.
Gastrin-releasing peptide (GRP) has recently been identified as an itch-specific neuropeptide in the spinal sensory system in mice, but there are no reports of the expression and distribution of GRP in the trigeminal sensory system in mammals. We characterized and compared GRP-immunoreactive (ir) ne
PMID 24254931

Modulation of glycinergic synaptic transmission in the trigeminal and hypoglossal motor nuclei by the nitric oxide-cyclicGMP signaling pathway.

Pose I1, Silveira V2, Damián A2, Higgie R2, Morales FR2.Author information 1Departamento de Fisiología, Facultad de Medicina, UDELAR, Montevideo, Uruguay. Electronic address: ipose@fmed.edu.uy.2Departamento de Fisiología, Facultad de Medicina, UDELAR, Montevideo, Uruguay.AbstractIn a previous work we found that nitric oxide (NO) and cyclicGMP (cGMP) inhibit glutamatergic synaptic transmission in trigeminal motoneurons (MnV). Here we study the actions of the NO/cGMP signaling pathway on glycinergic synaptic transmission in trigeminal and hypoglossal motoneurons (MnXII) in brain stem slices of neonatal rats. Glycinergic inhibitory postsynaptic currents (IPSCs) were recorded in MnV by stimulation of the supratrigeminal nucleus (SuV) and in MnXII by stimulation of the nucleus of Roller. The NO donor DETA/NONOate (DETA/NO) reduced the amplitude of the IPSC to 58.1±4.2% of control values in MnV. In the presence of YC-1, a modulator of guanylate cyclase that acts as a NO sensitizer, lower and otherwise ineffective concentrations of DETA/NO induced a reduction of the IPSC to 47.2±15.6%. NO effects were mimicked by 8 bromo cyclicGMP (8BrcGMP). They were accompanied by an increase in the paired pulse facilitation (PPF) and in the failure rate of evoked IPSCs. 8BrcGMP did not modify the glycinergic currents elicited by exogenous glycine. In MnXII the IPSCs were also reduced by NO donors and 8BrcGMP to 52.9±6.3% and 45.9±4% of control values, respectively. In these neurons, but not in MnV, we also observed excitatory postsynaptic actions of NO donors. We propose that the differences between the two motor pools may be due to a differential development of the nitrergic system in the two nuclei. Our data show that NO, through its second messenger cGMP, reduces inhibitory glycinergic synaptic transmission in both MnV and MnXII. For MnV, evidence in favor of presynaptic inhibition of glycine release is presented. Given our previous data together with the current results, we propose that the NO/cGMP signaling pathway participates pre- and postsynaptically in the combined regulation of MnV and MnXII activities in motor acts in which they participate.
Neuroscience.Neuroscience.2014 May 16;267:177-86. doi: 10.1016/j.neuroscience.2014.02.048. Epub 2014 Mar 10.
In a previous work we found that nitric oxide (NO) and cyclicGMP (cGMP) inhibit glutamatergic synaptic transmission in trigeminal motoneurons (MnV). Here we study the actions of the NO/cGMP signaling pathway on glycinergic synaptic transmission in trigeminal and hypoglossal motoneurons (MnXII) in br
PMID 24626159

Effects of intravenous metamizole on ongoing and evoked activity of dura-sensitive thalamic neurons in rats.

Sokolov AY1, Lyubashina OA2, Sivachenko IB3, Panteleev SS4.Author information 1Laboratory of Cortico-Visceral Physiology, Pavlov Institute of Physiology of the Russian Academy of Sciences, 6 Nab. Makarova, St. Petersburg 199034, Russia; Department of Neuropharmacology, Valdman Institute of Pharmacology, First St. Petersburg Pavlov State Medical University, 6/8 Lev Tolstoy Street, St. Petersburg 197022, Russia. Electronic address: alexey.y.sokolov@gmail.com.2Laboratory of Cortico-Visceral Physiology, Pavlov Institute of Physiology of the Russian Academy of Sciences, 6 Nab. Makarova, St. Petersburg 199034, Russia; Department of Neuropharmacology, Valdman Institute of Pharmacology, First St. Petersburg Pavlov State Medical University, 6/8 Lev Tolstoy Street, St. Petersburg 197022, Russia. Electronic address: olga@kolt.infran.ru.3Laboratory of Cortico-Visceral Physiology, Pavlov Institute of Physiology of the Russian Academy of Sciences, 6 Nab. Makarova, St. Petersburg 199034, Russia. Electronic address: AVANS_d@mail.ru.4Laboratory of Cortico-Visceral Physiology, Pavlov Institute of Physiology of the Russian Academy of Sciences, 6 Nab. Makarova, St. Petersburg 199034, Russia; Department of Neuropharmacology, Valdman Institute of Pharmacology, First St. Petersburg Pavlov State Medical University, 6/8 Lev Tolstoy Street, St. Petersburg 197022, Russia. Electronic address: panteleev@kolt.infran.ru.AbstractMigraine and tension-type headache (TTH) are the most common forms of primary headaches. A general key mechanism underlying development of both the diseases is the trigeminal system activation associated with the ascending nociceptive transmission via the trigemino-thalamo-cortical pathway. The ventroposteromedial (VPM) nucleus is a key thalamic structure, receiving afferent inflow from the craniofacial region; it holds the third-order neurons responsible for conveying sensory information from the extra- and intracranial nociceptors to the cortex. The VPM is currently seen as a therapeutic target for various antimigraine medications, which is shown to reduce the VPM neuronal excitability. A non-opioid analgesic metamizole is widely used in some countries for acute treatment of migraine or TTH. However, the precise mechanisms underlying anticephalgic action of metamizole remain unclear. The objective of our study performed in the rat model of trigemino-durovascular nociception was to evaluate the effects of intravenously administered metamizole on ongoing and evoked firing of the dura-sensitive VPM neurons. The experiments were carried out on rats under urethane-chloralose anesthesia. Cumulative administration of metamizole (thrice-repeated intravenous infusion of 150mg/kg performed 30min apart) in 56% of cases produced a suppression of both the ongoing activity of the thalamic VPM neurons and their responses to dural electrical stimulation. Although the inhibitory effect was prevailing, a number of VPM neurons were indifferent to the administration of metamizole. These data suggest that one of the main components of neural mechanism underlying anticephalgic action of metamizole is suppression of the thalamo-cortical nociceptive transmission associated with trigemino-vascular activation.
European journal of pharmacology.Eur J Pharmacol.2014 May 15;731:58-64. doi: 10.1016/j.ejphar.2014.03.006. Epub 2014 Mar 18.
Migraine and tension-type headache (TTH) are the most common forms of primary headaches. A general key mechanism underlying development of both the diseases is the trigeminal system activation associated with the ascending nociceptive transmission via the trigemino-thalamo-cortical pathway. The vent
PMID 24650732