Tooth pulp inflammation increases brain-derived neurotrophic factor expression in rodent trigeminal ganglion neurons

Tarsa, L.; Bałkowiec-Iskra, Ewa; Kratochvil, Frank J.; Jenkins, Victoria K.; McLean, Allan J.; Brown, Alexandra L.; Smith, Julie Ann; Baumgartner, J. Craig; Bałkowiec, Agnieszka

doi:10.1016/j.neuroscience.2010.03.002

Cited by 39 publications

(38 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IHC for BDNF on guinea pig trigeminal ganglion sections for the antibody positive control demonstrated that some neurons with small cell bodies were labeled strongly, consistent with reported results in the literature (Gunjigake et al 2006;Tarsa et al 2010) and indicating the efficacy of the antibody and IHC prototol used in our study (Fig. 5).…”

Section: Bdnf Expression In Human Cochleasupporting

confidence: 91%

“…For the positive control for the BDNF antibody, cryo-sections of guinea pig trigeminal ganglion fixed and sectioned by the same methods as those for human cochlea were subjected to IHC for BDNF. We used this tissue because, in rodent trigeminal ganglion, a substantial number of small BDNF-positive neurons have been constantly revealed (Gunjigake et al 2006;Tarsa et al 2010).…”

Section: Ihc and Immunocytochemistrymentioning

confidence: 99%

See 1 more Smart Citation

Expression of TrkB and BDNF in human cochlea—an immunohistochemical study

et al. 2011

View full text Add to dashboard Cite

Surgical human cochlear specimens were obtained during the removal of large posterior cranial fossa meningioma by a transcochlear approach in which the cochlea was removed for maximal exposure of the tumor and protection of important structures, such as the brainstem, cranial nerves, and pivotal blood vessels. The cochlear tissue was fixed and cryo-sectioned for tyrosine kinase receptor B (TrkB) and brain-derived neurotrophic factor (BDNF) immunohistochemistry. TrkB receptor protein was expressed in both neuronal somata and the processes of human spiral ganglion neurons (SGNs). In the human organ of Corti, TrkB immunoreactivity was mainly present in nerve fibers underneath outer hair cells. BDNF expression was found neither in the organ of Corti nor in the spiral ganglion of human cochlea. For antibody specificity and for control and comparative purposes, TrkB immunocytochemistry was performed in primary cultures of cochlear neuron/glia from adult guinea pig. Confocal laser scanning microscopy showed that TrkB was homogeneously distributed in the cytoplasm of both neuronal somata and axons. Knowledge of the expression of TrkB receptor in human cochlea should help to determine the target structures for neuron preservation in hearing-impaired patients. Our results indicate that the regeneration of SGNs under pathological conditions can be enhanced with BDNF/TrkB-based pharmaceutical or genetic strategies.

show abstract

Section: Bdnf Expression In Human Cochleasupporting

confidence: 91%

Section: Ihc and Immunocytochemistrymentioning

confidence: 99%

Expression of TrkB and BDNF in human cochlea—an immunohistochemical study

et al. 2011

View full text Add to dashboard Cite

show abstract

“…In addition, heat hyperalgesia in the whisker pad skin was depressed by daily application of neutralizing anti-NGF antibody to the inflamed lower lip or a nonspecific tyrosine kinase inhibitor K252a into TG ipsilateral to the inflamed lower lip. BDNF, which is TrkB ligand, is released from TG neurons by neuronal hyperexcitability (Buldyrev et al, 2006), and also tooth pulp inflammation significantly increased BDNF-and TRPV1-positive TG neurons (Tarsa et al, 2010). Because K252a inhibits tyrosine kinase, TrkB and TrkC inhibition by K252a may also be involved in depression of the heat hyperalgesia in whisker pad skin.…”

Section: Involvement Of Trpv1 In Heat Hyperalgesiamentioning

confidence: 99%

Nerve Growth Factor Contribution via Transient Receptor Potential Vanilloid 1 to Ectopic Orofacial Pain

Shinoda¹,

Asano²,

Omagari³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

It is well known that oral inflammation causes tenderness in temporomandibular joints or masseter muscles. The exact mechanism of such an orofacial ectopic hyperalgesia remains unclear. Here, we investigated the functional significance of interaction of nerve growth factor (NGF) and transient receptor potential vanilloid 1 (TRPV1) in relation to heat hyperalgesia in the whisker pad skin caused by complete Freund's adjuvant (CFA) injection into the lower lip. CFA injection induced heat hyperalgesia of the ipsilateral whisker pad skin. Moreover, it leads to enhancement of spontaneous activity and heat responses in trigeminal ganglion (TG) neurons that was elicited by heat stimulation of the whisker pad skin. The heat hyperalgesia was dose-dependently reversed by intraperitoneal TRPV1 antagonist administration, also diminished by neutralizing anti-NGF antibody administration into the lower lip and intraganglionic administration of K252a, a tyrosine kinase receptor inhibitor. Nerve fibers in bundle of mandibular nerve and TG neurons that innervates the whisker pad skin and lower lip both expressed labeled NGF, which was administrated into the lower lip. Moreover, the NGF concentrations in ophthalmic-maxillary and mandibular divisions of the TG increased after CFA injection into the lower lip. The number of TRPV1-positive neurons that innervates the whisker pad skin and lower lip was increased after CFA injection into the lower lip, and this increase was annulled by anti-NGF administration. The present findings suggest that inflammation in the lower lip induces release of NGF that regulates TRPV1 expression in TG neurons. This TRPV1 overexpression may underlie ectopic heat hyperalgesia in the whisker pad skin.

show abstract

“…Previous studies by our group indicate that BDNF is a candidate mediator of plasticity at first-order synapses in trigeminal nociceptive pathways (Buldyrev et al, 2006), with implications for pathophysiology of migraine and other primary headaches (Latremoliere and Woolf, 2009). Our recent studies show that inflammation within peripheral endings of trigeminal nociceptors dramatically upregulates BDNF in trigeminal ganglion (TG) neurons in vivo (Tarsa et al, 2010). However, the cellular mechanisms underlying the inflammation-induced BDNF upregulation remain unknown.…”

mentioning

confidence: 99%

Tumor necrosis factor-α increases brain-derived neurotrophic factor expression in trigeminal ganglion neurons in an activity-dependent manner

2011

Self Cite

View full text Add to dashboard Cite

Many chronic trigeminal pain conditions, such as migraine or temporo-mandibular disorders, are associated with inflammation within peripheral endings of trigeminal ganglion (TG) sensory neurons. A critical role in mechanisms of neuroinflammation is attributed to proinflammatory cytokines, such as interleukin-1β and tumor necrosis factor-α (TNFα) that also contribute to mechanisms of persistent neuropathic pain resulting from nerve injury. However, the mechanisms of cytokine-mediated synaptic plasticity and nociceptor sensitization are not completely understood. In the present study, we examined the effects of TNFα on neuronal expression of brain-derived neurotrophic factor (BDNF), whose role in synaptic plasticity and sensitization of nociceptive pathways is well documented. We show that 4-and 24-hr treatment with TNFα increases BDNF mRNA and protein, respectively, in neuron-enriched dissociated cultures of rat TG. TNFα increases the phosphorylated form of the cyclic adenosine monophosphate-responsive element binding protein (CREB), a transcription factor involved in regulation of BDNF expression in neurons, and activates transcription of BDNF exon IV (former exon III) and, to a lesser extent, exon VI (former exon IV), but not exon I. TNFα-mediated increase in BDNF expression was accompanied by increase in calcitonin gene-related peptide (CGRP), which is consistent with © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.Corresponding author: Dr. Agnieszka Balkowiec, Department of Integrative Biosciences, Oregon Health and Science University School of Dentistry, 611 S.W. Campus Drive, Portland, OR 97239; Phone: (503) 418-0190; Fax: (503) 494-8554; balkowie@ohsu.edu. All experimental protocols are available in a detailed, step-by-step format upon request from Dr. Ewa Bałkowiec-Iskra (ebalkowiec@wum.edu.pl).. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Research Highlights:1. BDNF mRNA and protein are upregulated in trigeminal ganglion neurons by TNF-α 2. TNF-α upregulates BDNF expression in a promoter-selective manner 3. TNF-α upregulation of BDNF expression is potentiated by neuronal activity and cAMP 4. TNF-α upregulation of BDNF expression depends on sodium channels and p38-MAPK 5. These data have implications for BDNF-dependent sensory plasticity NIH Public Access Vitkovic et al., 2000;Boulanger, 2009;Carpentier and Palmer, 2009). Thus, identifying the mechanisms that underlie neuro-immune interactions could become fundamental to understanding how the nervous system functions under physiological conditions and what goes awry in the disorders whose pa...

show abstract

Tooth pulp inflammation increases brain-derived neurotrophic factor expression in rodent trigeminal ganglion neurons

Cited by 39 publications

References 63 publications

Expression of TrkB and BDNF in human cochlea—an immunohistochemical study

Expression of TrkB and BDNF in human cochlea—an immunohistochemical study

Nerve Growth Factor Contribution via Transient Receptor Potential Vanilloid 1 to Ectopic Orofacial Pain

Tumor necrosis factor-α increases brain-derived neurotrophic factor expression in trigeminal ganglion neurons in an activity-dependent manner

Contact Info

Product

Resources

About