Capsaicin-evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation

Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin‐sensitive sensory neurons and the involvement of certain inflammatory mediators derived...

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Published in:	The European journal of neuroscience Vol. 14; no. 7; pp. 1113 - 1120
Main Authors:	Flores, Christopher M., Leong, Anthony S., O. Dussor, Gregory, Hargreaves, Kenneth M., Kilo, Sonja
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Science Ltd 01.10.2001
Subjects:	Animals Bradykinin - pharmacology Calcimycin - pharmacology Calcitonin Gene-Related Peptide - metabolism Calcium - metabolism Capsaicin - analogs & derivatives Capsaicin - pharmacology Dinoprostone - pharmacology Disease Models, Animal Dose-Response Relationship, Drug exocytosis Histamine - pharmacology in vitro superfusion Inflammation Mediators - metabolism Ionophores - pharmacology Male Mouth Mucosa - drug effects Mouth Mucosa - innervation Mouth Mucosa - metabolism Neurogenic Inflammation - chemically induced Neurogenic Inflammation - metabolism Neurogenic Inflammation - physiopathology neuropeptide nociceptor Nociceptors - drug effects Nociceptors - metabolism Organ Culture Techniques pain Pain Measurement - drug effects Potassium Chloride - pharmacology Rats Rats, Sprague-Dawley sensory neuron Serotonin - pharmacology Trigeminal Nerve - drug effects Trigeminal Nerve - metabolism
ISSN:	0953-816X, 1460-9568
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Abstract	Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin‐sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene‐related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 µm), to the superfusion buffer resulted in a significant, concentration‐dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 µm). The specific, capsaicin receptor antagonist, capsazepine (300 µm), completely abolished the capsaicin‐evoked release of iCGRP while having no effect whatsoever on the potassium‐evoked release. Moreover, capsaicin‐evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor‐mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.
AbstractList	Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin‐sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene‐related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 µ m ), to the superfusion buffer resulted in a significant, concentration‐dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 m m ) or by the calcium ionophore A23187 (1 µ m ). The specific, capsaicin receptor antagonist, capsazepine (300 µ m ), completely abolished the capsaicin‐evoked release of iCGRP while having no effect whatsoever on the potassium‐evoked release. Moreover, capsaicin‐evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor‐mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation. Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin‐sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene‐related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 µm), to the superfusion buffer resulted in a significant, concentration‐dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 µm). The specific, capsaicin receptor antagonist, capsazepine (300 µm), completely abolished the capsaicin‐evoked release of iCGRP while having no effect whatsoever on the potassium‐evoked release. Moreover, capsaicin‐evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor‐mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation. Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague-Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10-300 microm), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 microm). The specific, capsaicin receptor antagonist, capsazepine (300 microm), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation. Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague-Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10-300 mu m), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50mm) or by the calcium ionophore A23187 (1 mu m). The specific, capsaicin receptor antagonist, capsazepine (300 mu m), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation. Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague–Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10–300 μM), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mM) or by the calcium ionophore A23187 (1 μM). The specific, capsaicin receptor antagonist, capsazepine (300 μM), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation. Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague-Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10-300 microm), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 microm). The specific, capsaicin receptor antagonist, capsazepine (300 microm), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures. Such attributes include the dependence upon capsaicin-sensitive sensory neurons and the involvement of certain inflammatory mediators derived therein, including calcitonin gene-related peptide (CGRP). However, there are also important differences between the trigeminal and spinal nervous systems, and the potential contributions of neurogenic processes to inflammatory disease within the trigeminal system have yet to be fully elucidated. We present here a model system that affords the ability to study mechanisms regulating the efferent functions of peptidergic terminals that may subserve neurogenic inflammation within the oral cavity. Freshly dissected buccal mucosa tissue from adult, male, Sprague-Dawley rats was placed into chambers and superfused with oxygenated, Krebs buffer. Serial aliquots of the egressing superfusate were acquired and analysed by radioimmunoassay for immunoreactive CGRP (iCGRP). Addition of the selective excitotoxin, capsaicin (10-300 microm), to the superfusion buffer resulted in a significant, concentration-dependent increase in superfusate levels of iCGRP. Similarly, release of iCGRP from the buccal mucosa could also be evoked by a depolarizing concentration of potassium chloride (50 mm) or by the calcium ionophore A23187 (1 microm). The specific, capsaicin receptor antagonist, capsazepine (300 microm), completely abolished the capsaicin-evoked release of iCGRP while having no effect whatsoever on the potassium-evoked release. Moreover, capsaicin-evoked release was dependent upon the presence of extracellular calcium ions and was significantly, though incompletely, attenuated by neonatal capsaicin denervation. Collectively, these data indicate that the evoked neurosecretion of iCGRP in response to capsaicin occurs via a vanilloid receptor-mediated, exocytotic mechanism. The model system described here should greatly facilitate future investigations designed to identify and characterize the stimuli that regulate the release of CGRP or other neurosecretory substances in isolated tissues. This system may also be used to elucidate the role of these mediators in the aetiology of inflammatory processes within the trigeminal field of innervation.
Author	Kilo, Sonja Leong, Anthony S. Flores, Christopher M. O. Dussor, Gregory Hargreaves, Kenneth M.
AuthorAffiliation	2 Department of Pharmacology, The University of Texas Health Science Center, San Antonio, TX 78229–3900, USA 1 Department of Endodontics, The University of Texas Health Science Center, San Antonio, TX 78229–3900, USA 3 Department of Restorative Sciences, University of Minnesota, Minneapolis, MN 55455, USA
AuthorAffiliation_xml	– name: 3 Department of Restorative Sciences, University of Minnesota, Minneapolis, MN 55455, USA – name: 1 Department of Endodontics, The University of Texas Health Science Center, San Antonio, TX 78229–3900, USA – name: 2 Department of Pharmacology, The University of Texas Health Science Center, San Antonio, TX 78229–3900, USA
Author_xml	– sequence: 1 givenname: Christopher M. surname: Flores fullname: Flores, Christopher M. organization: Department of Endodontics, The University of Texas Health Science Center, San Antonio, TX 78229-3900, USA – sequence: 2 givenname: Anthony S. surname: Leong fullname: Leong, Anthony S. organization: Department of Endodontics, The University of Texas Health Science Center, San Antonio, TX 78229-3900, USA – sequence: 3 givenname: Gregory surname: O. Dussor fullname: O. Dussor, Gregory organization: Department of Pharmacology, The University of Texas Health Science Center, San Antonio, TX 78229-3900, USA – sequence: 4 givenname: Kenneth M. surname: Hargreaves fullname: Hargreaves, Kenneth M. organization: Department of Endodontics, The University of Texas Health Science Center, San Antonio, TX 78229-3900, USA – sequence: 5 givenname: Sonja surname: Kilo fullname: Kilo, Sonja
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/11683903$$D View this record in MEDLINE/PubMed
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Notes	istex:70945C5C9462911D4CD18049A98EFC31A8D36883 ArticleID:EJN1736 ark:/67375/WNG-B9KT27QG-C On leave from, Institut für Physiologie und Experimentelle Pathophysiologie, Universitätsstrasse 17, D‐91054 Erlangen, Germany. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 On leave from, Institut für Physiologie und Experimentelle Pathophysiologie, Universitätsstrasse 17, D-91054 Erlangen, Germany.
OpenAccessLink	https://www.ncbi.nlm.nih.gov/pmc/articles/2814599
PMID	11683903
PQID	1808661750
PQPubID	23462
PageCount	8
ParticipantIDs	pubmedcentral_primary_oai_pubmedcentral_nih_gov_2814599 proquest_miscellaneous_72238241 proquest_miscellaneous_1808661750 pubmed_primary_11683903 crossref_primary_10_1046_j_0953_816x_2001_01736_x crossref_citationtrail_10_1046_j_0953_816x_2001_01736_x wiley_primary_10_1046_j_0953_816x_2001_01736_x_EJN1736 istex_primary_ark_67375_WNG_B9KT27QG_C
PublicationCentury	2000
PublicationDate	October 2001
PublicationDateYYYYMMDD	2001-10-01
PublicationDate_xml	– month: 10 year: 2001 text: October 2001
PublicationDecade	2000
PublicationPlace	Oxford, UK
PublicationPlace_xml	– name: Oxford, UK – name: France
PublicationTitle	The European journal of neuroscience
PublicationTitleAlternate	Eur J Neurosci
PublicationYear	2001
Publisher	Blackwell Science Ltd
Publisher_xml	– name: Blackwell Science Ltd
References	Brain, S.J., Morris, H., MacIntyre, I. (1985) Calcitonin gene-related peptide is a potent vasodilator. Nature, 313, 54-56. Docherty, R.J., Yeats, J.C., Piper, A.S. (1997) Capsazepine block of voltage-activated calcium channels I adult rat dorsal root ganglion neurons in culture. Br. J. Pharmacol., 121, 1461-1467. Jancsó, G., Kiraly, E., Jancsó-Gábor, A. (1977) Pharmacologically induced selective degeration of chemosensitive primary sensory neurons. Nature, 270, 741-743. Escott, K.J., Beattie, D.T., Connor, H.E., Brain, S.D. (1995) Trigeminal ganglion stimulation increases facial skin blood flow in the rat: a major role for calcitonin gene-related peptide. Brain Res., 669, 93-99. Soinila, J., Salo, A., Unsitalo, H., Yanaihara, N., Happole, O. (1989) CGRP-immunoreactive sensory nerve fibers in the submandibular gland of the rat. Histochemistry, 91, 455-460. Györfi, A., Fazekas, Á., Fehér, E., Ender, F., Rosivall, L. (1996) Effects of streptozotocin-induced diabetes on neurogenic inflammation of gingivomucosal tissue in rat. J. Periodont. Res., 31, 249-255. Byers, M.R., Mecifi, K.B., Kimberly, C.L. (1987) Numerous nerves with calcitonin gene-related peptide-like immunoreactivity innervate junctional epithelium of rats. Brain Res., 419, 311-314. Caterina, M.J., Schumacher, M.A., Tominaga, M., Rosen, T.A., Levine, J.D., Julius, D. (1997) The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature, 389, 816-824. Karimian, M. & Ferrell, W.R. (1994) Plasma protein extravasation into the rat knee joint induced by calcitonin gene-related peptide. Neurosci. Lett., 166, 39-42. Leong, A.S., Kilo, S., Hargreaves, K.M., Flores, C.M. (1997) Modulation of capsaicin-evoked neuropeptide release by nicotine in the rat buccal musocsa. Soc. Neurosci. Abstr., 23, 874. Szallasi, A. & Blumberg, P.M. (1999) Vanilloid (capsaicin) receptors and mechanisms. Pharmacol. Rev., 51, 160-211. Barthold, P.M., Kylstra, A., Lawson, R. (1994) Substance P: an immunohistochemical and biochemical study in human gingival tissues. A role for neurogenic inflammation? J. Periodontol., 65, 1113-1121. Kilo, S., Harding-Rose, C., Hargreaves, K.M., Flores, C.M. (1997) Peripheral CGRP release as a marker for neurogenic inflammation: a model system for the study of neuropeptide secretion in rat paw skin. Pain, 73, 201-207. Goltz, F. (1874) Über gefässerweiternde Nerven. Pflueger Arch. Ges. Physiol., 9, 15. Györfi, A., Fazekas, Á., Irmes, F., Rosivall, L. (1995) Effect of substance P administration on vascular permeability in the rat oral mucosa and sublingual gland. J. Peridont. Res., 30, 181-185. Györfi, A., Fazekas, Á., Rosivall, L. (1992) Neurogenic inflammation and the oral mucosa. J. Clin. Periodontol., 19, 731-736. Gamse, R. & Saria, A. (1985) Potentiation of tachykinin-induced plasma protein extravasation by CGRP. Eur. J. Pharmacol., 114, 61-66. Ruokonen, H., Hietanen, J., Malmström, M., Sane, J., Häyrinen-Immonen, R., Hukkanen, M., Konttinen, Y.T. (1993) Peripheral nerves and mast cells in normal buccal mucosa. J. Oral Pathol. Med., 22, 30-34. Brain, S. & Williams, T. (1985) Inflammatory edema induced by synergism between CGRP and mediators of increased vascular permeability. Br. J. Pharmacol., 86, 855-860. Terenghi, G., Zhang, S.-Q., Under, W.G., Polak, J.M. (1986b) Morphological changes of sensory CGRP-immunoreactive and sympathetic nerves in peripheral tissues following chronic denervation. Histochemistry, 86, 89-95. Hargreaves, K.M., Bowles, W.R., Garry, G. (1992) An in vitro method to evaluate regulation of neuropeptide release. J. Endodontics, 18, 597-600. Luthman, J., Johansson, O., Ahlström, U., Kvint, S. (1988) Immunohistochemical studies of the neurochemical markers, CGRP, enkephalin, galanin, γ-MSH, NPY, PHI, proctolin, PTH, somatostatin, SP, VIP, tyrosine hydroxylase and neurofilament in nerves and cells of the human attached gingiva. Arch. Oral Biol., 33, 149-158. Silverman, J.D. & Kruger, L. (1989) Calcitonin gene-related peptide immunoreactive innervation of the rat head with emphasis on specialized sensory structures. J. Comp. Neurol., 280, 303-330. Kerezoudis, N.P., Olgart, L., Edwall, L. (1993) Evans blue extravasation in rat dental pulp and oral tissues induced by electrical stimulation of the inferior alveolar nerve. Arch. Oral Biol., 10, 893-901. Gazelius, B., Edwall, B., Olgart, L., Lundberg, J., Hokfelt, T., Fischer, J. (1987) Vasodilatory effects and coexistence of CGRP and substance P in sensory nerves of cat dental pulp. Acta Physiol. Scand., 130, 33-40. Hilliges, M., Hellman, M., Ahlström, U., Johansson, O. (1994) Immunohistochemical studies of neurochemical markers in normal human buccal mucosa. Histochemistry, 101, 235-244. Epstein, J.B. & Schubert, M.M. (1999) Oral mucositis in myelosuppressive cancer therapy. Oral Surg. Oral Med. Oral Pathol., 88, 273-276. Kato, J., Uddman, R., Sundler, F., Kurisu, K. (1998) Immunohistochemical study of the innervation of the boundary area of the hard and soft palates of the rat. Acta Anat., 163, 92-98. Linden, G.J., McKinnell, J., Shaw, C., Lundy, F.T. (1997) Substance P and neurokinin A in gingival crevicular fluid in periodontal health and disease. J. Clin. Periodontol., 24, 799-803. Nagata, E., Kondo, T., Ayasaka, N., Nakata, M., Tanaka, T. (1992) Immunohistochemical study of nerve fibres with substance P- or calcitonin gene-related peptide-like immunoreactivity in the junctional epithelium of developing rats. Arch. Oral Biol., 37, 655-662. Jancsó-Gábor, A. & Szolcsányi, J. (1972) Neurogenic inflammatory responses. J. Dent. Res., 51 (Suppl.), 264-269. Cruwys, S.C., Kidd, B.L., Mapp, P.I., Walsh, D.A., Blake, D.R. (1992) The effects of calcitonin gene-related peptide on formation of intra-articular oedema by inflammatory mediators. Br. J. Pharm., 107, 116-119. Holzer, P. (1988) Local effector function of capsaicin-sensitive sensory nerve endings: involvement of tachykinins, calcitonin gene-related peptide and other neuropeptides. Neuroscience, 24, 739-768. Fazekas, Á., Vindisch, K., Pósch, E., Györfi, A. (1990) Experimentally-induced neurogenic inflammationin the rat oral mucosa. J. Periodont. Res., 25, 276-282. Bowles, W.R., Oh, W., Sabino, M.L., Harding-Rose, C., Hargreaves, K.M. (1998) Development of an in vitro rat dental pulp superfusion model. J. Dent. Res., 77, 160. Chapman, L.F., Ramos, A.O., Goddell, H., Wolff, H.G. (1961) Neurohumoral features of afferent fibers in man. Arch. Neurol., 4, 617-650. Li, Y., Hsieh, S.T., Chien, H.F., Zhang, X., McArthur, J.C., Griffin, J.W. (1997) Sensory and motor denervation influence epidermal thickness in rat foot and glabrous skin. Exp. Neurol., 147, 452-462. Bayliss, W.M. (1901) On the origin from the spinal cord of the vaso-dilator fibres of the hindlimb, and on the nature of these fibres. J. Physiol. (Lond.), 26, 173-209. Kerezoudis, N.P., Olgart, L., Edwall, L. (1994) Involvement of substance P but not nitric oxide or calcitonin gene-related peptide in neurogenic plasma extravasation in rat incisor pulp and lip. Arch. Oral Biol., 39, 769-774. Fantini, F., Giannetti, A., Benassi, L., Cattaneo, V., Magnoni, C., Pincelli, C. (1995) Nerve growth factor receptor and neurochemical markers in human oral mucosa: an immunohistochemical study. Dermatology, 190, 186-191. Nadoolman, W., Duffy, V.B., Berger, A.M., Bartoshuk, L.M. (1994) Successive desensitization: a low pain/high dose technique for oral capsaicin delivery. Chem. Senses, 19, 494. Lewis, T., Harris, K.E., Grant, R.T. (1927) Influence of the cutaneous nerves on various reaction of the cutaneous vessels. Heart, 14, 1. Jancsó, N., Jancsó-Gábor, A., Szolcsányi, J. (1967) Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin. Br. J. Pharmacol., 31, 138-151. Terenghi, G., Polak, J.M., Rodrigo, J., Mulderry, P.K., Bloom, S.R. (1986a) Calcitonin gene-related peptide-immunoreactive nerves in the tonjue, epiglottis and pharynx of the rat: occurrence, distribution and origin. Brain Res., 365, 1-14. Kondo, T., Kido, M.A., Kiyoshima, T., Yamaza, T., Tanaka, T. (1995) An immunohistochemical and monastral blue-vascular labelling study on the involvement of capsaicin-sensitive sensory innervation of the junctional ipithelium in nurogenic plasma extravasation in the rat gingiva. Arch. Oral Biol., 10, 931-940. Wimalawansa, S.J. (1993) The effects of neonatal capsaicin on plasma levels and tissue contents of CGRP. Peptides, 14, 247-252. Donnerer, J., Schuligoi, R., Amann, R. (1992) Time-course of capsaicin-evoked release of calcitonin gene-related peptide from rat spinal cord in vitro. Effect of concentration and modulation by Ruthenium Red. Regul. Pept., 37, 27-37. Hammond, D.L. & Ruda, M.A. (1989) Developmental alterations in thermal nociceptive threshold and the distribution of immunoreactive calcitonin gene-related peptide and substance P after neonatal administration of capsaicin in the rat. Neurosci. Lett., 97, 57-62. Jackson, D.L., Garry, M., Engelstad, M., Geier, H., Hargreaves, K.M. (1992) An in vitro method to evaluate neuropeptide secretion from dental pulp. J. Dent. Res., 71, 178. Fazekas, Á., Györfi, A., Pósch, E., Jacab, G., Bártfai, Z., Rosivall, L. (1991) Effect of denervation on the neurogenic inflammation of the rat mandibular mucosa. Naunyn-Schmiedeberg's Arch. Pharmacol., 343, 393-398. Bongenhielm, U., Boissonade, F.M., Westermark, A., Robinson, P.P., Fried, K. (1999) Sympathetic nerve sprouting fails to occur in the trigeminal ganglion after peripheral nerve injury in the rat. Pain, 82, 183-288. Dussor, G.O., Leong, A.S., Gracia, N.B., Hargreaves, K.M., Arneric, S.P., Flores, C.M. (1998) Differential effects of neuronal nicotinic receptor agonists on capsaicin-evoked CGRP release from peripheral terminals of primary sensory neurons. Soc. Neurosci. Abstract., 24, 1625. Haber, J., Wattles, J., Crowby, M., Mandel, R., Kaunusi, J., Kent, R. (1993) Evidence for smoking as a major risk factor for periodontitis. J. Periodontol., 64, 16-23. Györfi, A., Fazekas, Á., 1995; 30 1993; 28 1993; 22 1993; 64 1874; 9 1989; 280 1992; 18 1988; 33 1999; 88 1992; 19 1999; 82 1992; 12 1996; 31 1994; 65 1994; 101 1997; 389 1997; 147 1991; 343 1961; 4 1999; 51 1972; 51 1994; 39 1998; 163 1986a; 365 1986b; 86 1977; 270 1927; 14 1986; 94 1991; 32 1997; 24 1995; 10 1997; 23 1992; 107 1992; 37 1985; 82 1985; 86 1992; 71 1998; 24 1987; 130 1901; 26 1995; 190 1993; 14 1994; 166 1997; 73 1989; 97 1990; 25 1967; 31 1994; 19 1989; 91 1997; 121 1993; 10 1995; 669 1992; 579 1987; 419 1985; 114 1985; 313 1988; 24 1998; 77 1968 e_1_2_6_53_1 e_1_2_6_32_1 e_1_2_6_30_1 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_59_1 Lewis T. (e_1_2_6_46_1) 1927; 14 e_1_2_6_11_1 e_1_2_6_17_1 e_1_2_6_55_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_62_1 e_1_2_6_43_1 e_1_2_6_20_1 e_1_2_6_41_1 Leong A.S. (e_1_2_6_45_1) 1997; 23 e_1_2_6_60_1 e_1_2_6_9_1 e_1_2_6_7_1 e_1_2_6_24_1 e_1_2_6_49_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_28_1 e_1_2_6_26_1 e_1_2_6_47_1 e_1_2_6_52_1 e_1_2_6_54_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_50_1 Jackson D.L. (e_1_2_6_34_1) 1992; 71 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_56_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_58_1 Dussor G.O. (e_1_2_6_14_1) 1998; 24 e_1_2_6_42_1 e_1_2_6_21_1 e_1_2_6_40_1 Nadoolman W. (e_1_2_6_51_1) 1994; 19 Szallasi A. (e_1_2_6_57_1) 1999; 51 e_1_2_6_8_1 Uddman R. (e_1_2_6_61_1) 1986; 94 Bowles W.R. (e_1_2_6_5_1) 1998; 77 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_29_1 e_1_2_6_44_1 Light A.R. (e_1_2_6_48_1) 1992 e_1_2_6_27_1
References_xml	– reference: Gazelius, B., Edwall, B., Olgart, L., Lundberg, J., Hokfelt, T., Fischer, J. (1987) Vasodilatory effects and coexistence of CGRP and substance P in sensory nerves of cat dental pulp. Acta Physiol. Scand., 130, 33-40. – reference: Kerezoudis, N.P., Olgart, L., Edwall, L. (1993) Evans blue extravasation in rat dental pulp and oral tissues induced by electrical stimulation of the inferior alveolar nerve. Arch. Oral Biol., 10, 893-901. – reference: Ruokonen, H., Hietanen, J., Malmström, M., Sane, J., Häyrinen-Immonen, R., Hukkanen, M., Konttinen, Y.T. (1993) Peripheral nerves and mast cells in normal buccal mucosa. J. Oral Pathol. Med., 22, 30-34. – reference: Li, Y., Hsieh, S.T., Chien, H.F., Zhang, X., McArthur, J.C., Griffin, J.W. (1997) Sensory and motor denervation influence epidermal thickness in rat foot and glabrous skin. Exp. Neurol., 147, 452-462. – reference: Hargreaves, K.M., Bowles, W.R., Garry, G. (1992) An in vitro method to evaluate regulation of neuropeptide release. J. Endodontics, 18, 597-600. – reference: Fantini, F., Giannetti, A., Benassi, L., Cattaneo, V., Magnoni, C., Pincelli, C. (1995) Nerve growth factor receptor and neurochemical markers in human oral mucosa: an immunohistochemical study. Dermatology, 190, 186-191. – reference: Dussor, G.O., Leong, A.S., Gracia, N.B., Hargreaves, K.M., Arneric, S.P., Flores, C.M. (1998) Differential effects of neuronal nicotinic receptor agonists on capsaicin-evoked CGRP release from peripheral terminals of primary sensory neurons. Soc. Neurosci. Abstract., 24, 1625. – reference: Hilliges, M., Hellman, M., Ahlström, U., Johansson, O. (1994) Immunohistochemical studies of neurochemical markers in normal human buccal mucosa. Histochemistry, 101, 235-244. – reference: Caterina, M.J., Schumacher, M.A., Tominaga, M., Rosen, T.A., Levine, J.D., Julius, D. (1997) The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature, 389, 816-824. – reference: Holzer, P. (1988) Local effector function of capsaicin-sensitive sensory nerve endings: involvement of tachykinins, calcitonin gene-related peptide and other neuropeptides. Neuroscience, 24, 739-768. – reference: Kilo, S., Harding-Rose, C., Hargreaves, K.M., Flores, C.M. (1997) Peripheral CGRP release as a marker for neurogenic inflammation: a model system for the study of neuropeptide secretion in rat paw skin. Pain, 73, 201-207. – reference: Bongenhielm, U., Boissonade, F.M., Westermark, A., Robinson, P.P., Fried, K. (1999) Sympathetic nerve sprouting fails to occur in the trigeminal ganglion after peripheral nerve injury in the rat. Pain, 82, 183-288. – reference: Gamse, R. & Saria, A. (1985) Potentiation of tachykinin-induced plasma protein extravasation by CGRP. Eur. J. Pharmacol., 114, 61-66. – reference: Jackson, D.L., Garry, M., Engelstad, M., Geier, H., Hargreaves, K.M. (1992) An in vitro method to evaluate neuropeptide secretion from dental pulp. J. Dent. Res., 71, 178. – reference: Györfi, A., Fazekas, Á., Fehér, E., Ender, F., Rosivall, L. (1996) Effects of streptozotocin-induced diabetes on neurogenic inflammation of gingivomucosal tissue in rat. J. Periodont. Res., 31, 249-255. – reference: Cruwys, S.C., Kidd, B.L., Mapp, P.I., Walsh, D.A., Blake, D.R. (1992) The effects of calcitonin gene-related peptide on formation of intra-articular oedema by inflammatory mediators. Br. J. Pharm., 107, 116-119. – reference: Leong, A.S., Kilo, S., Hargreaves, K.M., Flores, C.M. (1997) Modulation of capsaicin-evoked neuropeptide release by nicotine in the rat buccal musocsa. Soc. Neurosci. Abstr., 23, 874. – reference: Soinila, J., Salo, A., Unsitalo, H., Yanaihara, N., Happole, O. (1989) CGRP-immunoreactive sensory nerve fibers in the submandibular gland of the rat. Histochemistry, 91, 455-460. – reference: Hammond, D.L. & Ruda, M.A. (1989) Developmental alterations in thermal nociceptive threshold and the distribution of immunoreactive calcitonin gene-related peptide and substance P after neonatal administration of capsaicin in the rat. Neurosci. Lett., 97, 57-62. – reference: Györfi, A., Fazekas, Á., Irmes, F., Jakab, G., Süto, T., Rosivall, L. (1993) Role of substance P (SP) in development of symptoms of neurogenic inflammationin the oral mucosa of the rat. J. Peridont. Res., 28, 191-196. – reference: Nadoolman, W., Duffy, V.B., Berger, A.M., Bartoshuk, L.M. (1994) Successive desensitization: a low pain/high dose technique for oral capsaicin delivery. Chem. Senses, 19, 494. – reference: Byers, M.R., Mecifi, K.B., Kimberly, C.L. (1987) Numerous nerves with calcitonin gene-related peptide-like immunoreactivity innervate junctional epithelium of rats. Brain Res., 419, 311-314. – reference: Bowles, W.R., Oh, W., Sabino, M.L., Harding-Rose, C., Hargreaves, K.M. (1998) Development of an in vitro rat dental pulp superfusion model. J. Dent. Res., 77, 160. – reference: Jancsó-Gábor, A. & Szolcsányi, J. (1972) Neurogenic inflammatory responses. J. Dent. Res., 51 (Suppl.), 264-269. – reference: Luthman, J., Johansson, O., Ahlström, U., Kvint, S. (1988) Immunohistochemical studies of the neurochemical markers, CGRP, enkephalin, galanin, γ-MSH, NPY, PHI, proctolin, PTH, somatostatin, SP, VIP, tyrosine hydroxylase and neurofilament in nerves and cells of the human attached gingiva. Arch. Oral Biol., 33, 149-158. – reference: Silverman, J.D. & Kruger, L. (1989) Calcitonin gene-related peptide immunoreactive innervation of the rat head with emphasis on specialized sensory structures. J. Comp. Neurol., 280, 303-330. – reference: Escott, K.J., Beattie, D.T., Connor, H.E., Brain, S.D. (1995) Trigeminal ganglion stimulation increases facial skin blood flow in the rat: a major role for calcitonin gene-related peptide. Brain Res., 669, 93-99. – reference: Györfi, A., Fazekas, Á., Irmes, F., Rosivall, L. (1995) Effect of substance P administration on vascular permeability in the rat oral mucosa and sublingual gland. J. Peridont. Res., 30, 181-185. – reference: Tal, M. & Devor, M. (1992) Ectopic discharge in injured nerves: comparison of trigeminal and somatic afferents. Brain Res., 579, 148-151. – reference: Bayliss, W.M. (1901) On the origin from the spinal cord of the vaso-dilator fibres of the hindlimb, and on the nature of these fibres. J. Physiol. (Lond.), 26, 173-209. – reference: Fazekas, Á., Györfi, A., Pósch, E., Jacab, G., Bártfai, Z., Rosivall, L. (1991) Effect of denervation on the neurogenic inflammation of the rat mandibular mucosa. Naunyn-Schmiedeberg's Arch. Pharmacol., 343, 393-398. – reference: Barthold, P.M., Kylstra, A., Lawson, R. (1994) Substance P: an immunohistochemical and biochemical study in human gingival tissues. A role for neurogenic inflammation? J. Periodontol., 65, 1113-1121. – reference: Haber, J., Wattles, J., Crowby, M., Mandel, R., Kaunusi, J., Kent, R. (1993) Evidence for smoking as a major risk factor for periodontitis. J. Periodontol., 64, 16-23. – reference: Kondo, T., Kido, M.A., Kiyoshima, T., Yamaza, T., Tanaka, T. (1995) An immunohistochemical and monastral blue-vascular labelling study on the involvement of capsaicin-sensitive sensory innervation of the junctional ipithelium in nurogenic plasma extravasation in the rat gingiva. Arch. Oral Biol., 10, 931-940. – reference: Brain, S. & Williams, T. (1985) Inflammatory edema induced by synergism between CGRP and mediators of increased vascular permeability. Br. J. Pharmacol., 86, 855-860. – reference: Goltz, F. (1874) Über gefässerweiternde Nerven. Pflueger Arch. Ges. Physiol., 9, 15. – reference: Docherty, R.J., Yeats, J.C., Piper, A.S. (1997) Capsazepine block of voltage-activated calcium channels I adult rat dorsal root ganglion neurons in culture. Br. J. Pharmacol., 121, 1461-1467. – reference: Donnerer, J., Schuligoi, R., Amann, R. (1992) Time-course of capsaicin-evoked release of calcitonin gene-related peptide from rat spinal cord in vitro. Effect of concentration and modulation by Ruthenium Red. Regul. Pept., 37, 27-37. – reference: Jancsó, N., Jancsó-Gábor, A., Szolcsányi, J. (1967) Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin. Br. J. Pharmacol., 31, 138-151. – reference: Terenghi, G., Polak, J.M., Rodrigo, J., Mulderry, P.K., Bloom, S.R. (1986a) Calcitonin gene-related peptide-immunoreactive nerves in the tonjue, epiglottis and pharynx of the rat: occurrence, distribution and origin. Brain Res., 365, 1-14. – reference: Szallasi, A. & Blumberg, P.M. (1999) Vanilloid (capsaicin) receptors and mechanisms. Pharmacol. 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Snippet	Many of the physiological hallmarks associated with neurogenic inflammatory processes in cutaneous tissues are similarly present within orofacial structures....
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SubjectTerms	Animals Bradykinin - pharmacology Calcimycin - pharmacology Calcitonin Gene-Related Peptide - metabolism Calcium - metabolism Capsaicin - analogs & derivatives Capsaicin - pharmacology Dinoprostone - pharmacology Disease Models, Animal Dose-Response Relationship, Drug exocytosis Histamine - pharmacology in vitro superfusion Inflammation Mediators - metabolism Ionophores - pharmacology Male Mouth Mucosa - drug effects Mouth Mucosa - innervation Mouth Mucosa - metabolism Neurogenic Inflammation - chemically induced Neurogenic Inflammation - metabolism Neurogenic Inflammation - physiopathology neuropeptide nociceptor Nociceptors - drug effects Nociceptors - metabolism Organ Culture Techniques pain Pain Measurement - drug effects Potassium Chloride - pharmacology Rats Rats, Sprague-Dawley sensory neuron Serotonin - pharmacology Trigeminal Nerve - drug effects Trigeminal Nerve - metabolism
Title	Capsaicin-evoked CGRP release from rat buccal mucosa: development of a model system for studying trigeminal mechanisms of neurogenic inflammation
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