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Relevant bibliographies by topics / Superior Cervical Ganglion, pathology

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Academic literature on the topic 'Superior Cervical Ganglion, pathology'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Superior Cervical Ganglion, pathology"

1

Hisa, Yasuo, Toshiyuki Uno, Nobuhisa Tadaki, Kaori Umehara, Hitoshi Okamura, and Yasuhiko Ibata. "NADPH-diaphorase and nitric oxide synthase in the canine superior cervical ganglion." Cell and Tissue Research 279, no. 3 (February 1, 1995): 629–31. http://dx.doi.org/10.1007/s004410050322.

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Hisa, Yasuo, Toshiyuki Uno, Nobuhisa Tadaki, Kaori Umehara, Hitoshi Okamura, and Yasuhiko Ibata. "NADPH-diaphorase and nitric oxide synthase in the canine superior cervical ganglion." Cell & Tissue Research 279, no. 3 (March 1995): 629–31. http://dx.doi.org/10.1007/bf00318175.

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Dragoi, G. S., P. R. Melinte, D. Marinescu, I. Dinca, and M. M. Botoran. "Perenity of phenotype changes undergone by neuronal structures inside human superior cervical sympathetic ganglion. Implications in pathology." Romanian Journal of Legal Medicine 22, no. 1 (January 2014): 69–80. http://dx.doi.org/10.4323/rjlm.2014.69.

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Teclemariam-Mesbah, Rebecca, Andries Kalsbeek, Ruud M. Buijs, and Paul Pévet. "Oxytocin innervation of spinal preganglionic neurons projecting to the superior cervical ganglion in the rat." Cell and Tissue Research 287, no. 3 (February 20, 1997): 481–86. http://dx.doi.org/10.1007/s004410050772.

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Kasa, P., E. Dobo, and J. R. Wolff. "Cholinergic innervation of the mouse superior cervical ganglion: light-and electron-microscopic immunocytochemistry for choline acetyltransferase." Cell and Tissue Research 265, no. 1 (July 1991): 151–58. http://dx.doi.org/10.1007/bf00318149.

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Cancer, Hakan, Nobuaki Tamamaki, Uuji Handa, Minoru Hayashi, and Yoshiaki Nojyo. "Appearance of retrogradely labeled neurons in the rat superior cervical ganglion after injection of wheat-germ agglutinin-horseradish peroxidase conjugate into the contralateral ganglion." Cell and Tissue Research 262, no. 1 (October 1990): 53–57. http://dx.doi.org/10.1007/bf00327745.

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Yokota, H., H. Mukai, S. Hattori, K. Yamada, Y. Anzai, and T. Uno. "MR Imaging of the Superior Cervical Ganglion and Inferior Ganglion of the Vagus Nerve: Structures That Can Mimic Pathologic Retropharyngeal Lymph Nodes." American Journal of Neuroradiology 39, no. 1 (November 9, 2017): 170–76. http://dx.doi.org/10.3174/ajnr.a5434.

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Kameda, Yoko. "Signaling molecules and transcription factors involved in the development of the sympathetic nervous system, with special emphasis on the superior cervical ganglion." Cell and Tissue Research 357, no. 3 (April 26, 2014): 527–48. http://dx.doi.org/10.1007/s00441-014-1847-3.

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Loesch, Andrzej, Terry M. Mayhew, Helen Tang, Fernando V. Lobo Ladd, Aliny A. B. Lobo Ladd, Mariana Pereira de Melo, Andrea Almeida P. da Silva, and Antonio Augusto Coppi. "Stereological and allometric studies on neurons and axo-dendritic synapses in the superior cervical ganglia of rats, capybaras and horses." Cell and Tissue Research 341, no. 2 (July 2, 2010): 223–37. http://dx.doi.org/10.1007/s00441-010-1002-8.

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Zhang, En-Tan, Jens D. Mikkelsen, and Morten M�ller. "Tyrosine hydroxylase- and neuropeptide Y-immunoreactive nerve fibers in the pineal complex of untreated rats and rats following removal of the superior cervical ganglia." Cell and Tissue Research 265, no. 1 (July 1991): 63–71. http://dx.doi.org/10.1007/bf00318140.

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Dissertations / Theses on the topic "Superior Cervical Ganglion, pathology"

1

Morris, Teresa Ann. "Changes in adult rat superior cervical ganglion following axotomy." Miami University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=miami1281297277.

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Chiappini-Williamson, Christine. "Developmental Effects of Estrogen on the Superior Cervical Ganglion and Hypertension." Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1239913805.

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Zhu, Zheng. "Plasticity of Peripheral Neurons Following Axotomy of the Superior Cervical Ganglion." Miami University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=miami1324417326.

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Lin, Hung Wen. "Saturated fatty acids released from the rat superior cervical ganglion upon depolarization /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1691249441&sid=3&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (Ph. D.)--Southern Illinois University Carbondale, 2007.
"Department of Pharmacology." Keywords: Saturated fatty acids, Superior cervical ganglion, Depolarization Includes bibliographical references (p. 121-134). Also available online.

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Clowry, G. J. "Studies of neuronal connectivity in the superior cervical sympathetic ganglion of the rat." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382701.

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Walsh, Brian F. "Characterizing the regeneration of peripheral neurons: Re-innervation of the superior cervical ganglion." Miami University Honors Theses / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1272552715.

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Barrett, Curtis F. "Modulation of N-type Calcium Channels in Rat Superior Cervical Ganglion Neurons: A Dissertation." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/144.

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This thesis details my examination of several mechanisms for modulation of N-type calcium channels in neonatal rat superior cervical ganglion (SCG) neurons. The first part of this work characterizes cross-talk between two distinct mechanisms of modulation: readily-reversible inhibition induced by activation of heterotrimeric G-proteins (termed G-protein-mediated inhibition), and phosphorylation of the channel by protein kinase C (PKC). Data previously presented by other groups suggested that one effect of activating PKC is to prevent G-protein-mediated inhibition. The goal of this project was to confirm this hypothesis by testing functional competition between these two pathways. My findings show that G-protein-mediated inhibition blocks the effects of activating PKC, and that phosphorylation by PKC blocks G-protein-mediated inhibition, confirming that these two mechanisms are mutually exclusive. In addition, I investigated the effect of activating PKC on whole-cell barium currents in the absence of G-protein-mediated inhibition. When endogenous G-proteins were inactivated by dialyzing the cell with GDP-β-S, a guanine nucleotide that prevents activation of the G-protein's α subunit, activation of PKC with phorbol esters was without obvious effect on whole-cell current amplitude, fast and holding potential-dependent inactivation, and voltage-dependent activation, suggesting that PKC's principal role in modulating these currents is to prevent G-protein-mediated inhibition. From these results, I advanced Bean's 1989 model of reluctant and willing gating (induced by G-protein-mediated inhibition and relief of that inhibition, respectively). In this expanded model, reluctant channels, inhibited by G-proteins, are resistant to phosphylation by PKC (reluctant/P-resistant). Unmodulated channels are called willing/available, as they exhibit willing gating, and are available for either binding to a G-protein or phosphorylation by PKC. Finally, phosphorylation of a willing/available channel by PKC drives the channel into the willing/G-resistant state, in which the channel gates willingly, and is resistant to G-protein-mediated inhibition. These results are published in the Journal of General Physiology(2000; 115:277-286), and are presented in this thesis as Chapter II. In addition to membrane-delimited inhibition, N-type calcium channels are also subject to inhibition via a diffusible second-messenger pathway. In SCG neurons, this inhibition can be observed following stimulation of M1 muscarinic receptors by the agonist oxotremorine-M. Our lab previously hypothesized that the diffusible messenger involved might be the polyunsaturated fatty acid arachidonic acid (AA). To test this hypothesis, our lab examined the effect of bath-applied AA on whole-cell SCG calcium currents, and demonstrated that AA induces inhibition with similar properties as M1 muscarinic inhibition. An analysis of AA's effects on unitary N-type calcium currents, published by Liu and Rittenhouse in Journal of Physiology(2000; 525:391-404), revealed that this inhibition is mediated, at least in part, by both a significant increase in the occurrence of null-activity sweeps and a significant decrease in mean closed dwell time. Based on these results, our lab conducted an examination of AA's effects on whole-cell currents in SCG neurons, and found that AA-induced inhibition is mediated by an increase in holding potential-dependent inactivation and appears independent of AA metabolism. When I examined AA's effects in greater detail, I discovered that, in addition to inhibition, AA also appeared to cause significant enhancement of whole-cell currents. The results characterizing AA's general effects on whole-cell calcium currents in SCG neurons have been published in American Journal of Physiology - Cell Physiology(2001; 280:C1293-C1305). Because my finding that AA enhances whole-cell neuronal calcium currents revealed a novel pathway through which this current can be modulated, I proceeded to characterize this effect. My results showed that enhancement develops significantly faster than inhibition, suggesting different mechanisms or pathways. In addition, dialyzing the cell with BSA, a protein that binds fatty acids, blocked the majority of AA-induced inhibition, but did not reduce enhancement, suggesting that enhancement is independent of inhibition and might be mediated at an extracellular site. Using fatty acid analogs that cannot cross the cell membrane, I confirmed that enhancement occurs extracellularly. My data also indicate that AA-induced enhancement of whole-cell currents does not require metabolism of AA, consistent with enhancement being mediated directly by AA. I also examined the biophysical characteristics of enhancement, and found that both an increase in the voltage sensitivity of activation and an increase in activation kinetics underlie this effect. Finally, using both pharmacological agents and a recombinant cell line, I presented the first demonstration that AA enhances N-type calcium current. These findings are described in detail in a paper recently published in American Journal of Physiology - Cell Physiology(2001; 280:C1306-C1318), and are presented in this thesis as Chapter III. In our investigation of AA's effects on whole-cell calcium currents, we utilized a voltage protocol, in conjunction with pharmacology, to enhance the level of L-type current in these cells. Since whole-cell calcium currents in SCG neurons are comprised of mostly (80-85%) N-type current, with the remaining current comprised of mostly L-type current, this approach allowed us to examine both N- and L-type currents. When currents are recorded in the presence of 1 μM FPL 64174 (FPL), a benzoyl pyrrole L-type calcium channel agonist first described in 1989, stepping the membrane potential to -40 mV following a test pulse to +10 mV generates a slowly-deactivating ("tail") current. This tail current is made up entirely of L-type current, and allows us to readily investigate the effect of various modulatory mechanisms on this current type. Although FPL has been used for almost a decade to study L-type calcium currents, activity of FPL on N-type calcium currents has not been investigated. Because our lab routinely uses micromolar concentrations of FPL to measure whole-cell and unitary calcium currents in neuronal cells, I tested whether FPL has any effects on N-type calcium current. Therefore, I examined the effect of FPL on whole-cell calcium currents in an HEK 293 cell line that expresses recombinant N-type calcium channels. Application of 1 and 10 μM FPL caused significant, voltage-independent inhibition of currents, demonstrating that FPL inhibits N-type calcium current. Thus, at micromolar concentrations, FPL is not selective for L-type calcium current, and any examination of its effects on whole-cell calcium currents should take this into account. The results describing FPL's effects on L- and N-type calcium currents are included in a manuscript currently in preparation, and are presented as Chapter IV.

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SAKANAKA, MASAHIRO, SHIGERU KOBAYASHI, MINORU UEDA, TOSHIO SHIGETOMI, KENICHI KOSAKI, HIDEAKI KAGAMI, and YOSHIYUKI HIRAMATSU. "THE LOCALIZATION OF BASIC FIBROBLAST GROWTH FACTOR (FGF-2) IN RAT SUBMANDIBULAR GLANDS." Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/16076.

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9

Zhang, Chunyi. "Properties of an opioid-mediated inhibition evoked by preganglionic axons in the superior cervical ganglion of the cat." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41800.

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Immunohistochemical studies have shown opioid peptides in sympathetic ganglia and preganglionic neurons. An inhibitory action of opioids has been demonstrated in some central and peripheral synapses. However, a physiological role of endogenous opioids in sympathetic ganglia has not been well characterized. The present study investigated endogenous opioid action in the SCG of the cat. The results obtained show that an endogenous opioid is released from preganglionic axon terminals, in a frequency range that matches the natural activity of sympathetic preganglionic neurons, and inhibits ganglionic transmission by acting on post-synaptic opiate receptors of the $ mu$ and $ delta$ subtypes coupled to PTX-sensitive G protein. The size of the store of the endogenous opioid in the preganglionic axon terminals is small and readily exhaustible. Protein synthesis and axonal transport are required for maintenance of the store. The opioid inhibition is under control of the PKC system. This study provides the first thorough characterization of the properties of an opioid-mediated inhibitory mechanism in a well-defined synapse.

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10

Vogl, Christian. "Effects of the antiepileptic drug levetiracetam on synaptic transmission and presynaptic voltage-dependent Ca²+ channel activity in superior cervical ganglion neurones." Thesis, University of Reading, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558790.

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Levetiracetam (LEV) is a prominent antiepileptic drug (AED) with an unknown mechanism of action. Within this thesis, electrophysiological, biochemical and imaging approaches were combined to investigate potential effects of LEV on action potential (AP) -dependent synaptic transmission and presynaptic voltage-dependent Ca2+ channel (VDCC) activity in superior cervical ganglion neurons (SCGNs). The putative role of LEV's molecular target, synaptic vesicle protein 2A (SV2A) in mediating LEV effects was investigated using the R-enantiomer, UCB L060, which exerts a lOOO-fold lower SV2A binding affinity than LEV. In these experiments, LEV inhibited synaptic transmission in SCG model synapses in a time-dependent manner, significantly reducing excitatory postsynaptic potential (EPSP) amplitudes and surface areas when applied for 2:30 min in comparison to UCB L060. In isolated SCGNs and recombinantly expressed Cav2.2 channels in HEK293 cells, LEV pretreatment (2:1 h), but not acute external application, significantly inhibited whole-cell IBa- Antibody labelling of SV2A in SCGNs revealed that the protein was predominantly expressed in close proximity to the plasma membrane and did not appear to redistribute or change its total expression in response to LEV pretreatment. Intracellular LEV application significantly inhibited IBa rapidly after establishing the whole-cell configuration to an extent comparable to that following LEV pretreatment; however, neither pretreatment nor intracellular application of UCB L060 produced any inhibitory effects in these experiments, which indicates an intracellular site of action. Under physiological conditions, LEV reduced both, fast and slow AP after- hyperpolarisations in a Ca2+ -dependent manner but did not affect the AP waveform or resting membrane potential. Additionally, LEV increased AP latency and slowed the repolarisation rates in a Ca2+-independent manner, suggesting further mechanisms associated with reduced excitability . Taken together, the presented results identify presynaptic VDCCs as targets for the archetypal SV2A ligand, LEV, potentially acting via an SV2A-dependent, intracellular pathway to inhibit presynaptic Ca2+ influx.

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Books on the topic "Superior Cervical Ganglion, pathology"

1

Hodaie, Mojgan. The effect of patterns of electrical stimulation on the expression of the preprotachykinin gene in rat superior cervical ganglion neurons. Ottawa: National Library of Canada, 1994.

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2

Schwenk, Karen L. The role of afferent input to the Superior Cervical Ganglion in the plasticity of cerebrovascular axons. 1995.

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Shafer, Andrew J. Plasticity of calcitonin gene-related peptide immunoreactive axons in the rat superior cervical ganglion following infusion of nerve growth factor. 1998.

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McClenahan, Maureen F., and William Beckman. Pain Management Techniques. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190217518.003.0011.

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This chapter provides a broad review of various interventional pain management procedures with a focus on indications, anatomy, and complications. Specific techniques reviewed include transforaminal epidural steroid injection, lumbar sympathetic block, stellate ganglion block, cervical and lumbar radiofrequency ablation, gasserian ganglion block, sacroiliac joint injection, celiac plexus block, lateral femoral cutaneous nerve block, ilioinguinal block, lumbar medial branch block, obturator nerve block, ankle block, occipital nerve block, superior hypogastric plexus block, spinal cord stimulation, and intrathecal drug delivery systems. The chapter reviews contrast agents, neurolytic agents, botulinum toxin use, corticosteroids, and ziconotide pharmacology and side effects in addition to diagnosis and management of local anesthetic toxicity syndrome. It also discusses indications for neurosurgical techniques including dorsal root entry zone lesioning. In addition, information on radiation safety and the use of anticoagulants with neuraxial blocks is covered.

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Book chapters on the topic "Superior Cervical Ganglion, pathology"

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Jenkner, F. L. "Superior Cervical Ganglion." In Electric Pain Control, 63–68. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-3447-4_14.

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Bando, Hideki, Shinji Fuse, Atsushi Saito, and Yasuo Hisa. "Superior Cervical Ganglion." In Neuroanatomy and Neurophysiology of the Larynx, 67–72. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55750-0_8.

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Jankovic, Danilo. "Superior Cervical Ganglion Block." In Regional Nerve Blocks in Anesthesia and Pain Therapy, 201–9. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05131-4_14.

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Loreto, Andrea, and Jonathan Gilley. "Axon Degeneration Assays in Superior Cervical Ganglion Explant Cultures." In Methods in Molecular Biology, 15–24. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0585-1_2.

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Gilley, Jonathan, and Andrea Loreto. "Microinjection of Superior Cervical Ganglion Neurons for Studying Axon Degeneration." In Methods in Molecular Biology, 25–39. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0585-1_3.

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Dawson, Chandler R., Wen-hua Zhang, and Odeon Briones. "Superior Cervical Ganglion in Experimental Herpes Simplex Virus Eye Disease." In Herpetic Eye Diseases, 23–26. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5518-9_4.

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Perlman, Robert L., Anne L. Cahill, and Joel Horwitz. "Protein Phosphorylation and Phospholipid Metabolism in the Superior Cervical Ganglion." In Neurobiology of Acetylcholine, 111–20. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5266-2_9.

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Kása, P., E. Dobó, and J. R. Wolff. "GABAergic Action on Cholinergic Axon Terminals in the Superior Cervical Ganglion." In GABA Outside the CNS, 83–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76915-3_6.

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Kiraly, M., E. Tribollet, M. Dolivo, and J. J. Dreifuss. "A Presynaptic Action of Vasopressin in the Superior Cervical Ganglion of the Rat." In Histochemistry and Cell Biology of Autonomic Neurons and Paraganglia, 334–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72749-8_58.

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Horwitz, Joel, Sofia Tsymbalov, and Robert L. Perlman. "Metabolism of Inositol-Containing Phospholipids in the Superior Cervical Ganglion of the Rat." In Inositol and Phosphoinositides, 637–42. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5184-2_41.

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