Relevant bibliographies by topics / Geniculate ganglion

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  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Geniculate ganglion'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Geniculate ganglion"

1

Magliulo, Giuseppe, Francesca Alla, Giovanna Colicchio, and Guido Trasimeni. "Geniculate Ganglion Meningioma." Skull Base 20, no. 03 (October 30, 2009): 185–88. http://dx.doi.org/10.1055/s-0029-1242196.

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Semaan, Maroun T., William H. Slattery, and Derald E. Brackmann. "Geniculate Ganglion Hemangiomas." Otology & Neurotology 31, no. 4 (June 2010): 665–70. http://dx.doi.org/10.1097/mao.0b013e3181d2f021.

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Lahlou, Ghizlene, Yann Nguyen, Francesca Yoshie Russo, Evelyne Ferrary, Olivier Sterkers, and Daniele Bernardeschi. "Geniculate Ganglion Tumors." Otolaryngology–Head and Neck Surgery 155, no. 5 (August 9, 2016): 850–55. http://dx.doi.org/10.1177/0194599816661482.

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Chung, C. J., Suresh Mukherji, Lynn Fordham, William Boydston, and Roger Hudgins. "Geniculate ganglion meningioma." Pediatric Radiology 27, no. 11 (November 17, 1997): 847–49. http://dx.doi.org/10.1007/s002470050252.

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Mu, Xiaofei, Yong Quan, Jiang Shao, Jianfeng Li, Haibo Wang, and Ruozhen Gong. "Enlarged Geniculate Ganglion Fossa." Academic Radiology 19, no. 8 (August 2012): 971–76. http://dx.doi.org/10.1016/j.acra.2012.03.025.

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Ayajiki, Kazuhide, Toshiki Tanaka, Tomio Okamura, and Noboru Toda. "Evidence for nitroxidergic innervation in monkey ophthalmic arteries in vivo and in vitro." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (October 1, 2000): H2006—H2012. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h2006.

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In anesthetized monkeys, electrical stimulation (ES) of the pterygopalatine or geniculate ganglion dilated the ipsilateral ophthalmic artery (OA). The induced vasodilatation was unaffected by phentolamine but potentiated by atropine. Intravenous N G-nitro-l-arginine (l-NNA) abolished the response, which was restored byl-arginine. Hexamethonium-abolished vasodilator responses induced solely by geniculate ganglionic stimulation. Thel-NNA constricted OA; l-arginine reversed the effect. Destruction of the pterygopalatine ganglion constricted the ipsilateral artery. Helical strips of OA isolated under deep anesthesia from monkeys, denuded of endothelium, responded to transmural ES with relaxations, which were abolished by tetrodotoxin and l-NNA but were potentiated by atropine. It is concluded that neurogenic vasodilatation of monkey OA is mediated by nerve-derived nitric oxide (NO), and the nerve is originated from the ipsilateral pterygopalatine ganglion that is innervated by cholinergic neurons from the brain stem via the geniculate ganglion. The OA appears to be dilated by mediation of NO continuously liberated from nerves that receive tonic discharges from the vasomotor center. Acetylcholine liberated from postganglionic cholinergic nerves would impair the release of neurogenic NO.
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Grigaliunas, Arturas, Robert M. Bradley, Donald K. MacCallum, and Charlotte M. Mistretta. "Distinctive Neurophysiological Properties of Embryonic Trigeminal and Geniculate Neurons in Culture." Journal of Neurophysiology 88, no. 4 (October 1, 2002): 2058–74. http://dx.doi.org/10.1152/jn.2002.88.4.2058.

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Neurons in trigeminal and geniculate ganglia extend neurites that share contiguous target tissue fields in the fungiform papillae and taste buds of the mammalian tongue and thereby have principal roles in lingual somatosensation and gustation. Although functional differentiation of these neurons is central to formation of lingual sensory circuits, there is little known about electrophysiological properties of developing trigeminal and geniculate ganglia or the extrinsic factors that might regulate neural development. We used whole cell recordings from embryonic day 16 rat ganglia, maintained in culture as explants for 3–10 days with neurotrophin support to characterize basic properties of trigeminal and geniculate neurons over time in vitro and in comparison to each other. Each ganglion was cultured with the neurotrophin that supports maximal neuron survival and that would be encountered by growing neurites at highest concentration in target fields. Resting membrane potential and time constant did not alter over days in culture, whereas membrane resistance decreased and capacitance increased in association with small increases in trigeminal and geniculate soma size. Small gradual differences in action potential properties were observed for both ganglion types, including an increase in threshold current to elicit an action potential and a decrease in duration and increase in rise and fall slopes so that action potentials became shorter and sharper with time in culture. Using a period of 5–8 days in culture when neural properties are generally stable, we compared trigeminal and geniculate ganglia and revealed major differences between these embryonic ganglia in passive membrane and action potential characteristics. Geniculate neurons had lower resting membrane potential and higher input resistance and smaller, shorter, and sharper action potentials with lower thresholds than trigeminal neurons. Whereas all trigeminal neurons produced a single action potential at threshold depolarization, 35% of geniculate neurons fired repetitively. Furthermore, all trigeminal neurons produced TTX-resistant action potentials, but geniculate action potentials were abolished in the presence of low concentrations of TTX. Both trigeminal and geniculate neurons had inflections on the falling phase of the action potential that were reduced in the presence of various pharmacological blockers of calcium channel activation. Use of nifedipine, ω-conotoxin-MVIIA and GVIA, and ω-agatoxin-TK indicated that currents through L-, N-, and P/Q- type calcium channels participate in the action potential inflection in embryonic trigeminal and geniculate neurons. The data on passive membrane, action potential, and ion channel characteristics demonstrate clear differences between trigeminal and geniculate ganglion neurons at an embryonic stage when target tissues are innervated but receptor organs have not developed or are still immature. Therefore these electrophysiological distinctions between embryonic ganglia are present before neural activity from differentiated receptive fields can influence functional phenotype.
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Usrey, W. Martin, John B. Reppas, and R. Clay Reid. "Specificity and Strength of Retinogeniculate Connections." Journal of Neurophysiology 82, no. 6 (December 1, 1999): 3527–40. http://dx.doi.org/10.1152/jn.1999.82.6.3527.

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Retinal ganglion cells and their target neurons in the principal layers of the lateral geniculate nucleus (LGN) of the thalamus have very similar, center-surround receptive fields. Although some geniculate neurons are dominated by a single retinal afferent, others receive both strong and weak inputs from several retinal afferents. In the present study, experiments were performed in the cat that examined the specificity and strength of monosynaptic connections between retinal ganglion cells and their target neurons. The responses of 205 pairs of retinal ganglion cells and geniculate neurons with overlapping receptive-field centers or surrounds were studied. Receptive fields were mapped quantitatively using a white-noise stimulus; connectivity was assessed by cross-correlating the retinal and geniculate spike trains. Of the 205 pairs, 12 were determined to have monosynaptic connections. Both the likelihood that cells were connected and the strength of connections increased with increasing similarity between retinal and geniculate receptive fields. Connections were never found between cells with <50% spatial overlap between their centers. The results suggest that although geniculate neurons often receive input from several retinal afferents, these multiple afferents represent a select subset of the retinal ganglion cells with overlapping receptive-field centers.
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Dožić, A., M. Ćetković, S. Marinković, D. Mitrović, M. Grujičić, M. Mićović, and M. Milisavljević. "Vascularisation of the geniculate ganglion." Folia Morphologica 73, no. 4 (November 28, 2014): 414–21. http://dx.doi.org/10.5603/fm.2014.0063.

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Casas-Rodera, Pablo, Luis Lassaletta, María José Sarriá, and Javier Gavilán. "Haemangiomas of the Geniculate Ganglion." Acta Otorrinolaringologica (English Edition) 58, no. 7 (January 2007): 327–30. http://dx.doi.org/10.1016/s2173-5735(07)70359-9.

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Dissertations / Theses on the topic "Geniculate ganglion"

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Koudelka, Juraj. "Determining TrkB intracellular signalling pathways required for specific aspects of gustatory development." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8830.

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Neurotrophins BDNF and NT4 influence the development of the rodent gustatory system. Despite binding to the same receptor, TrkB, they have different roles. BDNF is chemo-attractive for gustatory neurons and regulates gustatory neuron targeting and number during development. NT4 regulates gustatory neuron number earlier in development than BDNF, but it is not chemo-attractive and does not regulate gustatory neuron targeting. To elucidate the mechanisms that regulate these processes we have examined which TrkB intracellular signalling pathways are required for specific aspects of gustatory development by studying the effect of specific point mutations in TrkB docking sites. We found that the TrkB/Shc docking site is involved in regulating the survival of geniculate ganglion neurons as a point mutation in this adaptor site (TrkbS/S) caused large losses of these neurons as early as E12.5. These losses were exacerbated throughout development until after birth. A point mutation in the TrkB/PLCγ (TrkbP/P) docking site did not cause loss of geniculate ganglion neurons at any point during development. Animals with a point mutation in both docking sites (TrkbD/D) caused a further decrease in neuron numbers compared to animals with a mutation in only one of the docking sites, similarly to what has previously been shown in Trkb null animals. We concluded that the TrkB/Shc docking site is crucial for determining the survival of geniculate ganglion neurons during mouse gustatory development, while the TrkB/PLCγ docking site does not affect the neuronal survival directly and likely plays a role in maintenance of these neurons. Examining the targeting of geniculate ganglion afferents into the tongue revealed large deficits in innervated neural bud and taste bud numbers in TrkbS/S animals both before and after birth. This was concluded to be reflecting the lack of neuronal survival in this ganglion, a result that was mirrored in TrkbD/D animals. TrkbP/P animals, on the other hand, exhibited a developmental delay in innervation. This was indicated by a low amount of innervated neural buds following the initial innervation period, which was compensated for by a large increase in the number of innervated taste buds by birth. By adulthood, the numbers of taste buds present on the tongues of TrkbP/P animals reached normal numbers compared to control animals. This suggested that the TrkB/PLCγ docking site is involved primarily in innervation. Finally, we examined the morphology of taste buds in newly born and adult animals. We found that the low amount of geniculate ganglion afferents innervating the tongue in TrkbS/S and TrkbD/D animals caused a decrease in size of taste buds. This effect was seen to be partially rescued by adulthood in TrkbS/S animals but not in TrkbD/D animals due to lack of viability. The morphology of taste buds was unaffected in TrkbP/P animals until adulthood, at which point the size of the taste buds was increased. These results are in agreement with previous findings showing dependency of taste bud morphology on the amount of innervation. Overall, our findings show a differential role of TrkB adaptor sites in gustatory development. Despite activated by the same ligands, the docking sites on this receptor are able to exert different influence on signalling pathways downstream of TrkB affecting neuronal survival, targeting and morphology of taste buds.
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Dursun, Ilknur. "The Effects Of Early Postnatal Ethanol Intoxication On Retina Ganglion Cell Morphology And The Development Of Retino-geniculate Projections In Mice." Phd thesis, METU, 2010. http://etd.lib.metu.edu.tr/upload/12613011/index.pdf.

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Experimental and clinical data have documented the adverse effects of perinatal ethanol intoxication on peripheral organs and the central nervous system. There is little known, however, about potential damaging effects of perinatal ethanol on the developing visual system. The purpose of this study was to examine the effects of neonatal ethanol intoxication on RGC morphology, estimate the total number of neurons in RGC layer and dorsolateral geniculate nucleus (dLGN), and on the eye-specific fiber segregation in the dLGN), in YFP and C57BL/6 mice pups. Ethanol (3 g/kg/day) was administered by intragastric intubation throughout postnatal days (PD) 3-20 or 3-10. Intubation control (IC) and untreated control (C) groups were included. Blood alcohol concentration (BAC) was measured in separate groups of pups on PD3, PD10, and PD20 at 4 different time points, 1, 1.5, 2 and 3 h after the second intubation. Numbers neurons in the RGCs and dLGN were quantified on PD10, PD20 using unbiased stereological procedures. The RGC images were taken using a confocal microscope and images were traced using Neurolucida software. On PD9, intraocular injections of cholera toxin-
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Haner, Cheryl. "Novel Roles for Reelin in Retinogeniculate Targeting." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2233.

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In the developing visual system, the axon of a pre-synaptic cell must be guided to a post-synaptic partner. Retinal ganglion cells (RGCs) in the eye are an excellent model to study this process. Multiple classes exist that respond to specific types of light input, and these project to different destinations in the brain that process distinct types of information. The RGC axons that navigate to the lateral geniculate nucleus (LGN) do so in a class-specific manner. Axons from RGCs that mediate non-image forming functions innervate the ventral LGN (vLGN) and the intergeniculate leaflet (IGL). Axons from RGCs that process image-forming information bypass these regions to innervate the dorsal LGN (dLGN). The extracellular protein reelin was identified as a potential factor in RGC axonal targeting of the vLGN and IGL, and the reeler mutant mouse used to study the effects of its functional absence. Anterograde labeling of RGCs and their axons with Cholera toxin B (CTB) revealed reduced patterns of retinal innervation to the vLGN and IGL in mutant mice. Moreover, the absence of functional reelin resulted in axons incorrectly growing into inappropriate regions of the thalamus. We identified these misrouted axons as those of the intrinsically photosensitive RGCs (ipRGCS), a class of RGCs known to project to the affected subnuclei. In contrast to defects in ipRGC targeting, no deficits were seen in retinogeniculate or corticothalamic projections in classes of axons that normally target the dLGN. Immunohistochemistry did not reveal any effects of the absence of the functional reelin on the LGN cytoarchitecture, which is unlike many other brain regions altered in the reeler. In summary, results suggest that intact reelin is required for class-specific retinogeniculate targeting to the vLGN and IGL. The defects are likely to be in targeting and not in neuronal positioning.
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Book chapters on the topic "Geniculate ganglion"

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Darrouzet, V., F. Gharbi, C. De Bonfils, C. Rognon, and J. P. Bebear. "Herpes Zoster of the Geniculate Ganglion: Therapeutic Concepts." In The Facial Nerve, 493–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85090-5_195.

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Moriyama, H., K. Shimada, N. Goto, S. Shigihara, and R. F. Gasser. "Observations on the Geniculate Ganglion in Adult Human Dissections." In The Facial Nerve, 117–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85090-5_34.

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Nakashima, Michio, Mamiko Yanaura, Satoshi Yamada, and Satoru Shiono. "Optical Recording of Neural Signals in Rat Geniculate Ganglion." In Olfaction and Taste XI, 409. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68355-1_162.

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Jenkner, F. L. "Trigeminal (with supraorbital; maxillary and infraorbital; mandibular and mental nerves) and Glossopharyngeal Nerves with relatively rare Neuralgias of Geniculate Ganglion (Hunt) and Sphenopalatine Ganglion (Sluder)." In Electric Pain Control, 86–92. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-3447-4_19.

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Hedges III, Thomas R. "Optic Tract and Lateral Geniculate Body Field Defects." In Visual Fields. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195389685.003.0014.

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Lesions affecting the optic tracts can cause a variety of neuro-ophthalmic signs. Not only are the visual field defects distinctive, but they are also associated with findings that encompass pupillary physiology and retinal nerve fiber anatomy as well as central and peripheral ocular motor function. For example, a patient with a lesion in the region of an optic tract might have: incongruous, macular splitting hemianopia, the details of which require careful performance and interpretation of the visual fields; band atrophy of the optic nerve and retinal nerve fiber layer; a relative afferent pupillary defect; and a third nerve palsy. Indeed, much of neuroophthalmology can be learned from a thorough understanding of lesions involving the optic tracts. Therefore, a review of the neuro-anatomy of this region is very important. After the fibers of the retinal ganglion cells decussate in the chiasm, they pass into the optic tract. The pupillary fibers leave the tract before the lateral geniculate body and travel to the midbrain. On magnetic resonance imaging (MRI) scans the hilum of the lateral geniculate nucleus (LGN) can be seen where it abuts the lateral recess of the ambient cistern. The lateral and superior borders of the LGN are sharply defined by the white matter of the optic radiations. As the visual fibers make their way through the tract, there is a 90° nasal rotation. As a result, the two groups of homonymous fibers from both upper retinas, which represent the lower field, rotate to a medial position in the tract. The lower homonymous retinal fibers rotate laterally. The macular fibers (which are the vast majority) occupy a wedge-shaped area between the medial and lateral portions. The fibers from the corresponding retinal areas begin to associate themselves as they progress through the optic tract. The midbrain is nearby and the third cranial nerve lies just below the optic tract. Because of this imperfect match of corresponding retinal areas from each eye in the tract, the field defects due to lesions affecting the optic tract are incongruous— that is, the defect is different in each eye when demonstrated by the same-size test object.
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Wesley, Ralph E. "Management of Facial Palsy." In Surgery of the Eyelid, Lacrimal System, and Orbit. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780195340211.003.0017.

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Facial palsy can devastate patients. Facial appearance can be grossly distorted by the sagging of half the face, often accompanied by drooling of food and saliva from the paralyzed lip. Blurred vision and ocular pain from exposure and dryness may interfere with the patient’s ability to perform an occupation or interact socially. Many patients with facial palsy experience depression or severe discouragement. Effective management of ocular problems by the ophthalmologist can have a profound effect on the patient’s rehabilitation. The ophthalmologist managing facial palsy should be aware of wide-ranging choices in the medical and surgical armamentarium to treat facial palsy. This chapter describes the varying clinical dimensions of facial palsy so that treatment can be individualized for effective management. The facial nerve (cranial nerve VII) has four important functions: 1. The facial motor nucleus controls muscles of facial expression, including the orbicularis oculi. 2. The superior salivatory nucleus sends parasympathetic fibers for lacrimal gland secretion and salivary secretion. 3. The nucleus solitarius receives sensory fibers of taste for the anterior two thirds of the tongue. 4. The trigeminal sensory nucleus receives sensory fibers for a small portion of the external ear. Facial motor fibers constitute about 58% of the 7,000 fibers of the facial nerve, while preganglionic fibers for tearing and salivation represent about 24%. The facial nerve leaves the cerebellopontine angle caudal to the trigeminal nerve adjacent to the nervus intermedius and then enters the internal auditory canal of the temporal bone. Large lesions of cranial nerve VII or VIII may cause loss of corneal sensation from pressure on the trigeminal nerve. The 30-mm course through the temporal bone is the longest interosseous course of any cranial nerve, which makes the facial nerve vulnerable to swelling. Three branches leave the facial nerve within the temporal bone. The first, and most important, arises at the geniculate ganglion just as the nerve makes a sharp bend, or genu, to head posteriorly. These fibers for lacrimal and palatine gland secretion constitute the greater superficial petrosal nerve carrying lacrimal secretory fibers to the pterygopalatine ganglion.
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