Disease relevance of Trigeminal Ganglion

• The incidence of trigeminal ganglion infection after corneal inoculation of guinea pigs with thymidine kinase-negative mutants of herpes simplex virus was markedly reduced compared to infection after inoculation of thymidine kinase-positive virus [1].
• The vasoactive molecule serotonin, implicated in the pathogenesis of migraine, coexists with substance P in some terminals of the central nervous system and is present within the trigeminal ganglia [2].
• The tract reached the level of the trigeminal ganglion by E10.0 but did not enter the ganglion until after E12 [3].
• Collectively, the results indicate that the activation of the hypothalamic pituitary adrenal axis plays an important role in stimulating IL-6 expression and HSV-1 reactivation in the trigeminal ganglion following hyperthermic stress of mice [4].
• We compared the levels of latent pseudorabies virus (PRV) DNA in trigeminal ganglia (TG) of pigs after intranasal inoculation of different PRV strains by using quantitative DNA PCR [5].

High impact information on Trigeminal Ganglion

• Release of the predicted calcitonin gene-related peptide from cultured rat trigeminal ganglion cells [6].
• Thymidine kinase-positive virus, however, replicated well in ocular tissues as well as in trigeminal ganglion [1].
• Particularly striking was restoration of near-normal trigeminal ganglion replication and neurovirulence of an ICP34.5 mutant in IFN-alpha/betaR-/- mice [7].
• The replication of these viruses was examined in eyes and trigeminal ganglia for 1-7 d after corneal inoculation in mice with null mutations (-/-) in interferon receptors (IFNR) for type I IFNs (IFN-alpha/betaR), type II IFN (IFN-gammaR), and both type I and type II IFNs (IFN-alpha/beta/gammaR) [7].
• Intracisternal A and C particles in mouse neurons: a thin-section study of normal trigeminal ganglion and C1300 neuroblastoma [8].

Chemical compound and disease context of Trigeminal Ganglion

• Cyanoketone blocked the stress-induced rise in IL-6 mRNA and protein expression in the trigeminal ganglion latently infected with HSV-1 [4].
• Judging from the number and intensity of the labeling, the superior cervical ganglion and the trigeminal ganglion and dorsal root ganglion at level C2 contributed most to the innervation [9].
• Novobiocin and coumermycin A1 inhibit viral replication and the reactivation of herpes simplex virus type 1 from the trigeminal ganglia of latently infected mice [10].
• HSV-1 mutant viruses missing the invariant intron-terminal 5'-G(T/C) or 3'-AG dinucleotides were analyzed for LAT formation during lytic infection in vitro, when only the 2-kb LAT is produced, and during latency in mouse trigeminal ganglia, where both LATs are expressed [11].
• We also investigated the effects of these same mediators on the c-GMP and/or c-AMP concentrations in HSV-latently infected trigeminal ganglion cells and in acyclovir-suppressed, HSV-infected neuroblastoma cells [12].

Biological context of Trigeminal Ganglion

• Selective 5-HT1D alpha serotonin receptor gene expression in trigeminal ganglia: implications for antimigraine drug development [13].
• At E14 in vivo, the number of trigeminal neurons undergoing apoptosis was significantly greater in bcl-2(-/-) embryos, and there were significantly fewer neurons in the trigeminal ganglia of bcl-2(-/-) embryos at E16 and E18 [14].
• The excessive cell death led to a progressive decline in the number of proliferating cells without a significant change in the fraction of dividing cells and total number of neurons, indicating that the neuronal deficit of NT-3-/- mice was caused by cell death of trigeminal ganglion progenitors [15].
• 125I-peptide YY (PYY) was used to localize and characterize NPY receptor binding sites in trigeminal ganglia, DRG, and spinal cord of the rat, rabbit, and monkey [16].
• The protective efficacy of the IFN-alpha 1 transgene antagonized viral replication, as evidenced by the reduction of the viral gene transcripts (infected cell polypeptide 27, thymidine kinase, and viral protein 16) and viral load in eyes and trigeminal ganglia during acute infection [17].

Anatomical context of Trigeminal Ganglion

• NT-3, NT-4, and more prominently BDNF, induce neurite outgrowth from explant cultures of the E10 trigeminal ganglia but no neurites are induced by NGF, despite the expression of trkA [18].
• In lumbar dorsal root ganglia and trigeminal ganglia, abundant LNGFR mRNA was found in all neurons with strong 125I-NGF labeling and on additional neurons lacking high-affinity NGF-binding sites [19].
• Previous studies have shown that most neurons in cultures established during the early stages of neurogenesis in the embryonic mouse trigeminal ganglion are supported by BDNF whereas most neurons cultured from older ganglia survive with NGF [20].
• Early sensory neurons cultured from the trigeminal ganglia of bcl-2-/- embryos at embryonic day 11 (E11) and E12 underwent this change more slowly than trigeminal neurons of wild-type embryos of the same ages [21].
• Pharmacological experiments using selective Y1 and Y2 receptor antagonists suggest that Y2 is the prominent NPY receptor subtype expressed in trigeminal ganglia neurons, DRG neurons, and spinal cord [16].

Associations of Trigeminal Ganglion with chemical compounds

• A rapid capsaicin-activated current in rat trigeminal ganglion neurons [22].
• We found that sumatriptan effectively prevented the induction of sensitization (i.e., increased spontaneous firing; increased neuronal sensitivity to intracranial mechanical stimuli) in central trigeminovascular neurons (recorded in the dorsal horn), but not in peripheral trigeminovascular neurons (recorded in the trigeminal ganglion) [23].
• Sensory axons from the trigeminal ganglion (V) innervate cephalic blood vessels and use the preprotachykinin gene products, substance P (SP) and neurokinin A (NKA), as putative neurotransmitters conveying nociceptive information [24].
• Glutamate receptor subunits GluR5 and KA-2 are coexpressed in rat trigeminal ganglion neurons [25].
• An ipsilateral increase in Evans blue and 125I-BSA was found in the dura, eyelids, lips and gingival mucosa, and snout following electrical stimulation of the rat trigeminal ganglion [26].

Gene context of Trigeminal Ganglion

• The trigeminal ganglia of NGF/p75(-/-) mice, like those of NGF/p75(+/+) mice, have increased levels of NGF protein and display a concomitant ingrowth of sympathetic axons [27].
• Neurotrophin-4 is a target-derived neurotrophic factor for neurons of the trigeminal ganglion [28].
• Whereas there was no significant difference between the number of pyknotic nuclei in trkA-/- and wild-type embryos at E11 and E12, there was a substantial increase in the number of pyknotic nuclei in the trigeminal ganglia of trkB-/- at these earlier stages [29].
• Presumptive dermal and epidermal cells from the maxillary territory of the embryonic mouse trigeminal ganglion were cultured in defined medium during the early stages of innervation when trigeminal neurons switch their survival dependence from NT-3 to NGF [30].
• The astrocytes in the CNS, the unmyelinated Schwann cells in the sciatic nerve, and the satellite cells in the trigeminal ganglion stained heavily with anti-GFAP antiserum [31].

Analytical, diagnostic and therapeutic context of Trigeminal Ganglion

• However, in IFN-alpha/betaR-/- or IFN-alpha/beta/gammaR-/- mice, growth of all mutants, including those with significantly impaired growth in cell culture, was enhanced by up to 1,000-fold in eyes and trigeminal ganglia [7].
• 3H-GEMSA autoradiography of the trigeminal ganglion localizes EC to the sensory neurons and not to white matter tracts there [32].
• In situ hybridization with a digoxigenin-labeled riboprobe specific for LAT detected an average of one to two LAT-positive cells in each positive 6-microns section of trigeminal ganglion [33].
• As determined by reverse transcriptase PCR, IFN-gamma and tumor necrosis factor alpha transcripts were present in trigeminal ganglia during both acute and latent HSV-1 infection [34].
• Finally, 17 delta Sty reactivated with normal kinetics from the trigeminal ganglia of latently infected mice in the explant cocultivation assay and egressed from tissue culture cells as efficiently as wild-type virus [35].

References