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Relevant bibliographies by topics / Trigeminal placode

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Academic literature on the topic 'Trigeminal placode'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Trigeminal placode"

1

Stark, M. R., J. Sechrist, M. Bronner-Fraser, and C. Marcelle. "Neural tube-ectoderm interactions are required for trigeminal placode formation." Development 124, no. 21 (November 1, 1997): 4287–95. http://dx.doi.org/10.1242/dev.124.21.4287.

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Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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2

Baker, C. V., and M. Bronner-Fraser. "Establishing neuronal identity in vertebrate neurogenic placodes." Development 127, no. 14 (July 15, 2000): 3045–56. http://dx.doi.org/10.1242/dev.127.14.3045.

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The trigeminal and epibranchial placodes of vertebrate embryos form different types of sensory neurons. The trigeminal placodes form cutaneous sensory neurons that innervate the face and jaws, while the epibranchial placodes (geniculate, petrosal and nodose) form visceral sensory neurons that innervate taste buds and visceral organs. In the chick embryo, the ophthalmic trigeminal (opV) placode expresses the paired homeodomain transcription factor Pax3 from very early stages, while the epibranchial placodes express Pax2. Here, we show that Pax3 expression in explanted opV placode ectoderm correlates at the single cell level with neuronal specification and with commitment to an opV fate. When opV (trigeminal) ectoderm is grafted in place of the nodose (epibranchial) placode, Pax3-expressing cells form Pax3-positive neurons on the same schedule as in the opV placode. In contrast, Pax3-negative cells in the grafted ectoderm are induced to express the epibranchial placode marker Pax2 and form neurons in the nodose ganglion that express the epibranchial neuron marker Phox2a on the same schedule as host nodose neurons. They also project neurites along central and peripheral nodose neurite pathways and survive until well after the main period of cell death in the nodose ganglion. The older the opV ectoderm is at the time of grafting, the more Pax3-positive cells it contains and the more committed it is to an opV fate. Our results suggest that, within the neurogenic placodes, there does not appear to be a two-step induction of ‘generic’ neurons followed by specification of the neuron to a particular fate. Instead, there seems to be a one-step induction in which neuronal subtype identity is coupled to neuronal differentiation.

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3

Baker, C. V., M. R. Stark, C. Marcelle, and M. Bronner-Fraser. "Competence, specification and induction of Pax-3 in the trigeminal placode." Development 126, no. 1 (January 1, 1999): 147–56. http://dx.doi.org/10.1242/dev.126.1.147.

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Placodes are discrete regions of thickened ectoderm that contribute extensively to the peripheral nervous system in the vertebrate head. The paired-domain transcription factor Pax-3 is an early molecular marker for the avian ophthalmic trigeminal (opV) placode, which forms sensory neurons in the ophthalmic lobe of the trigeminal ganglion. Here, we use collagen gel cultures and heterotopic quail-chick grafts to examine the competence, specification and induction of Pax-3 in the opV placode. At the 3-somite stage, the whole head ectoderm rostral to the first somite is competent to express Pax-3 when grafted to the opV placode region, though competence is rapidly lost thereafter in otic-level ectoderm. Pax-3 specification in presumptive opV placode ectoderm occurs by the 8-somite stage, concomitant with robust Pax-3 expression. From the 8-somite stage onwards, significant numbers of cells are committed to express Pax-3. The entire length of the neural tube has the ability to induce Pax-3 expression in competent head ectoderm and the inductive interaction is direct. We propose a detailed model for Pax-3 induction in the opV placode.

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4

Knabe, Wolfgang, Bastian Obermayer, Hans-Jürg Kuhn, Guido Brunnett, and Stefan Washausen. "Apoptosis and proliferation in the trigeminal placode." Brain Structure and Function 214, no. 1 (November 14, 2009): 49–65. http://dx.doi.org/10.1007/s00429-009-0228-2.

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5

McCabe, Kathryn L., and Marianne Bronner-Fraser. "PDGF signaling is critical for trigeminal placode formation." Developmental Biology 319, no. 2 (July 2008): 534. http://dx.doi.org/10.1016/j.ydbio.2008.05.246.

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6

McCabe, Kathryn L., and Marianne Bronner-Fraser. "Essential role for PDGF signaling in trigeminal placode formation." Developmental Biology 306, no. 1 (June 2007): 294. http://dx.doi.org/10.1016/j.ydbio.2007.03.066.

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7

McCabe, K. L., and M. Bronner-Fraser. "Essential role for PDGF signaling in ophthalmic trigeminal placode induction." Development 135, no. 10 (April 9, 2008): 1863–74. http://dx.doi.org/10.1242/dev.017954.

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8

McCabe, Kathryn L., Celia E. Shiau, and Marianne Bronner-Fraser. "Identification of candidate secreted factors involved in trigeminal placode induction." Developmental Dynamics 236, no. 10 (2007): 2925–35. http://dx.doi.org/10.1002/dvdy.21325.

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9

McCabe, Kathryn L., and Marianne Bronner. "Tetraspanin, CD151, is required for maintenance of trigeminal placode identity." Journal of Neurochemistry 117, no. 2 (February 24, 2011): 221–30. http://dx.doi.org/10.1111/j.1471-4159.2011.07190.x.

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10

McCabe, Kathryn L., and Marianne Bronner-Fraser. "An essential role for the tetraspanin, CD151, in trigeminal placode formation." Developmental Biology 331, no. 2 (July 2009): 510. http://dx.doi.org/10.1016/j.ydbio.2009.05.459.

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Dissertations / Theses on the topic "Trigeminal placode"

1

Reynolds, Stephanie Beth. "The Role of FGFR4 in Trigeminal Placode Cell Development." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1234.pdf.

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2

Xu, Hong. "Development of the maxillomandibular trigeminal placode in the chick embryo." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612197.

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3

Dude, Carolynn Marie. "Pax3 and the development of the avian ophthalmic trigeminal placode." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612069.

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4

Ball, Matthew K. "Function of the Notch/Delta Pathway in Ophthalmic Trigeminal Placode Development." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2122.

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The ophthalmic trigeminal placode (opV) is the birth place of one cell type of sensory neurons contributing to the trigeminal ganglion. Signals from the neural tube induce placodal identity within the surface ectoderm. Specified opV placode cells then up-regulate neuron differentiation markers and migrate to the ganglion. Several molecular pathways have been shown to act in opV placode cell development. Despite this, signals that specify individual neurons from within the opV placode remain unknown. However, it is known that components of the Notch signaling pathway are expressed in the opV placode. I tested the role of Notch signaling in opV placode development by separately inhibiting and over-activating the pathway. Using DAPT, an inhibitor of gamma-secretase, I inhibited Notch signaling in 13-15 somite stage chick embryo heads. Attenuated Notch signaling caused increased neuronal differentiation of opV cells at 13-15 somites. I also observed an increase in migratory opV placode (Pax3+) cells in the mesenchyme and expression of neuronal marker Islet1 in the ectoderm. Further, I activated Notch signaling by misexpressing the Notch intracellular domain (NICD) by in ovo electroporation of 10-12 somite stage chick embryos. This resulted in Pax3+ targeted cells failing to differentiate and remain instead in the ectoderm. Thus, Notch/Delta signaling plays an important role in selecting ophthalmic trigeminal cells to differentiate and migrate to the trigeminal ganglion.

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Lassiter, Rhonda Nicole. "The Role of Wnt Signaling in Development of the Ophthalmic Trigeminal Placode." BYU ScholarsArchive, 2006. https://scholarsarchive.byu.edu/etd/1297.

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Cranial placodes are ectodermal regions that contribute extensively to the vertebrate peripheral nervous system. The development of the ophthalmic trigeminal (opV) placode, which gives rise only to sensory neurons of the ophthalmic lobe of the trigeminal ganglion, is a well-studied model of sensory neuron development. While key differentiation processes have been characterized at the tissue and cellular levels, the molecules governing opV placode development have not been well described. This study identifies the canonical Wnt signaling pathway as a regulator of opV trigeminal placode development. Introducing dominant-negative TCF and dominant-active β-catenin expression constructs by in ovo electroporation, we have manipulated the canonical Wnt pathway within the opV placode domain and surrounding ectoderm of chick embryos. Inhibition of canonical Wnt signaling results in the failure of targeted cells to express or maintain Pax3 protein, the earliest known specific molecular marker of opV placode cells. Misexpression of dominant-active β-catenin as an activator of canonical Wnt signaling, however, is not sufficient to promote the opV placode cell fate. We conclude that canonical Wnt signaling is necessary for normal opV placode development, and propose that other molecular cues are required in addition to Wnt signaling to promote cells to an opV placode fate. Strategies for manipulating the Wnt pathway at the level of ligand and receptor are also reviewed. Because it is clear that Wnt signaling is not acting alone in early development of the opV placode, we have also begun to investigate additional signaling pathways, such as FGFs, that may be involved in these developmental processes.

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6

Lassiter, Rhonda Nicole Thomas. "The role of Wnt signaling in development of the ophthalmic trigeminal placode /." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1637.pdf.

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7

Adams, Jason Samuel. "Regulation of Sensory Neurogenesis in the Trigeminal Placode: Notch Pathway Genes, Pax3 Isoforms, and Wnt Ligands." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3144.

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This dissertation is divided into three chapters, each discussing the study of different regulatory molecules involved in sensory neurogenesis occurring in the trigeminal placode. Chapter one is a spatiotemporal description of Notch pathway genes in chick opV placode by stage-specific expression analysis, showing expression of many Notch pathway genes and effectors in the opV placode. Notch pathway gene expression is primarily confined to the ectoderm with highest expression of these genes at the beginning stages of peak neuronal differentiation. This information preceded studies of the functional roles that Notch signaling has in the opV placode and how it may affect the transcription factor, Pax3. Chapter two is a study of the transcription factor Pax3 and its role in opV placode development and sensory neuron differentiation. Pax3 is known to activate or repress gene transcription, and its activity may be dependent on the splice variant or isoform present. We show through RT-PCR that alternative splice forms of Pax3 are present at stages of chick development corresponding to cellular competence, cellular differentiation and ingression, and cellular aggregation. We have named these splice forms, Pax3V1 and Pax3V2. Using quantitative RT-PCR we show that Pax3V2 is consistently expressed at lower levels compared to Pax3 during cellular competence and differentiation. In order to determine the function of the three splice forms, we misexpressed them in the opV placode and analyzed the effect on neurogenesis. We looked at markers for neuronal differentiation of targeted cells after in ovo electroporation of Pax3, Pax3V1, and Pax3V2, which showed a significant difference between the control and each construct, but not between the groups of constructs. To enhance the process of neurogenesis we exposed the electroporated embryos to DAPT, a Notch signaling inhibitor that enhances sensory neurogenesis. Using this method we found that misexpression of Pax3 and Pax3V1 resulted in cells failing to differentiate, while Pax3V2 misexpression more closely resembles the neuronal differentiation seen in controls. These results show that the Pax3V2 isoform allows for neuronal differentiation of opV placodal cells after misexpression, while the Pax3 isoform and the Pax3V1 isoform block neuronal differentiation. Chapter three is a study of the necessity of Wnt signaling originating from the neural tube to induce Pax3 expression in the opV placode. A double knockout of Wnt1 and Wnt3a was produced to determine the necessity of these genes in opV placode development. Pax3 expression in the opV placode at E8.5 and E9.5 was markedly reduced in the double mutants when compared to wild type mice. This study shows that Wnt1 and Wnt3a genes are necessary for normal Pax3 expression, but that other signals may contribute to its induction.

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8

Bradshaw, James R. "The Role of Pax3 in Neuronal Differentiation of the Ophthalmic (OpV) Trigeminal Placode and Neural Tube during Chicken Embryonic Development." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1208.pdf.

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9

Hulet, Julie Louise. "The Effects of Inhibiting Wnt Secretion and Activity on Cranial And Neural Development." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/5503.

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Wnt signaling has been shown to have several roles in the development of sensory neurons, particularly in the ophthalmic portion of the trigeminal nerve. Many of these studies have relied on the conclusion that Wnt is necessary but not sufficient for the induction and maintenance of the neural precursor cells that develop in the ophthalmic placode. Wnt had been inhibited in the ophthalmic placode using a dominant negative t-cell factor (TCF) and resulted in the loss of Pax3 expression (indicative of undifferentiated placode cells) in all targeted cells, suggesting a loss of specification/commitment of these cells to the sensory neuron fate. This study aimed to build on that conclusion by identifying the source of Wnt signaling that allowed for the maintenance of these placode cells. To investigate this, chick embryo ex ovo cultures were used and treated with small molecule chemical Wnt inhibitors to globally knock out Wnt signaling. The embryos were then sectioned and stained for cell markers of undifferentiated placode and differentiated neural cells (Pax3 and Islet1, respectively). Also used was a conditional knockout of Porcn, a gene critical to post-transcriptional modification of the Wnt ligand, using Wnt1-cre as a driver; this allowed for the knockout of Wnt secretion from the dorsal neural tube as well as neural crest cells. The data showed a decrease in placode cell differentiation but did not indicate a necessity for Wnt in maintenance of the ophthalmic placode cells—there was no loss of Pax3 expressing cells in the ectoderm. This suggested that maintenance of the ophthalmic placode could be through alternate pathways. Data is also presented describing how loss of Porcn in Wnt1 expressing cells impacts craniofacial development, where the mouse mutant used in this study displayed the absence and underdevelopment of cranial neural crest structures.

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10

Voelkel, Jacob Eugene. "A Model for Sensory Neuron Development by FGF and Notch: A Multifactorial Approach." BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4122.

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The ophthalmic trigeminal placode (opV) exclusively gives rise to sensory neurons. A number of signaling pathways including Wnt, PDGF, FGF, and Notch are all involved in the progression of an undifferentiated cell in the opV placode to a proneural cell in the condensing opV ganglion. However, the regulatory relationships between these signal transduction pathways are still unknown. To determine if FGF activation acts to modulate Notch signaling in the sensory neurogenesis pathway, a novel multifactorial approach was employed: FGF signaling was inhibited in individual cells and globally with simultaneous inactivation of Notch signaling in chick embryos to investigate if FGF activation downregulates Notch thereby driving neurogenesis. These experiments resulted in few differentiating opV cells in the mesenchymal region of future ganglion formation suggesting an alternate regulatory relationship between FGF and Notch where either reduced Notch activity allows for FGFR4 expression (leading to FGF signaling and neurogenesis), or a parallel relationship where FGF and Notch act independently of one another to induce neurogenesis. To distinguish between these two possibilities Notch signaling was inhibited with DAPT, a gamma-secretase inhibitor, and assayed for FGFR4 mRNA expression. These results indicated FGFR4 is not upregulated by reduced Notch activity, suggesting that FGF and Notch act in parallel to promote neurogenesis. During these experiments it was observed that Notch inhibition resulted in an undefined ectoderm in the opV placode region. To investigate this, FGF and Notch were inhibited by SU5402, an FGF antagonist, and DAPT, and later sectioned and stained for Laminin. In DAPT treated embryos the basement membrane became highly fragmented, a remarkable observation not yet reported. From these data a proposed mechanism was established where activation of FGF with parallel downregulation of Notch leads to disruption of extracellular matrix proteins in the basement membrane resulting in fragmentation and subsequent delamination of differentiating opV placode cells.

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Books on the topic "Trigeminal placode"

1

Working in a very small place: The making of a neurosurgeon. New York: Norton, 1989.

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2

Working in a very small place: The making of a neurosurgeon. New York: Vintage Books, 1990.

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Book chapters on the topic "Trigeminal placode"

1

Field, Nicholas C., and Julie G. Pilitsis. "Trigeminal Neuropathic Pain." In Pain Neurosurgery, 149–56. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190887674.003.0019.

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Motor cortex stimulation is a surgical treatment for medically refractory trigeminal neuropathic pain, a syndrome often caused by nerve injury due to trauma, dental work, or previous surgery for trigeminal neuralgia. Preoperative planning includes pain assessment scales, psychological clearance, and functional magnetic resonance imaging (fMRI) to map the motor cortex. The patient undergoes a craniotomy with trial placement of an epidural electrode array, assisted by neuronavigation, phase reversal monitoring, and somatosensory evoked potential recordings. Less commonly, the electrodes are placed in the subdural space. Postoperative seizure is the most common complication, additionally there are risks for infection and hemorrhage. Programming of the device is performed and the patient undergoes permanent implantation of the system if they achieve a greater than 50% reduction in their pain. Further research is necessary to determine which patients will have the best response to therapy.

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Tandon, Nitin, and Konstantin V. Slavin. "Epilepsy, Functional, and Pain Neurosurgery." In Goodman's Neurosurgery Oral Board Review, 139–60. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190055189.003.0011.

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This chapter covers several aspects of the management of seizures and epilepsy relevant to a general neurosurgical practice. First, all candidates should know how to manage a patient presenting with a new-onset seizure or in status epilepticus with a brain lesion or after a craniotomy. Second, they are expected to be able to explain how to perform fundamental epilepsy procedures such as a temporal lobectomy for hippocampal sclerosis or resection of an epileptogenic lesion. Third, it is useful to have a clear process in place for mapping language and motor function for the resection of tumors located in the eloquent cortex. Lastly, the thought process behind developing an appropriate plan for the surgical management of movement disorders and the technical nuances of managing such cases are discussed. Historically, surgery for pain has been a large part of general neurosurgical practice. A variety of destructive and decompressive interventions have been developed over the years, and a number of comprehensive textbooks have summarized neurosurgical involvement with management of all kinds of medically refractory pain syndromes. It is included in the core neurosurgical education curriculum and is an integral part of neurosurgical knowledge that is tested during the oral board examination. Not surprisingly, cases involving complex pain conditions that require neurosurgical interventions may show up during examinations, and it is expected that examinees are comfortable performing these interventions and able to discuss indications, surgical details, outcomes and complications. Cases include trigeminal neuralgia, cordotomy versus morphine pain pump for cancer pain and a spinal cord stimulator.

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