Tags

Type your tag names separated by a space and hit enter

Calcitonin gene-related peptide enhances release of native brain-derived neurotrophic factor from trigeminal ganglion neurons.
J Neurochem. 2006 Dec; 99(5):1338-50.JN

Abstract

Activity-dependent plasticity in nociceptive pathways has been implicated in pathomechanisms of chronic pain syndromes. Calcitonin gene-related peptide (CGRP), which is expressed by trigeminal nociceptors, has recently been identified as a key player in the mechanism of migraine headaches. Here we show that CGRP is coexpressed with brain-derived neurotrophic factor (BDNF) in a large subset of adult rat trigeminal ganglion neurons in vivo. Using ELISA in situ, we show that CGRP (1-1000 nM) potently enhances BDNF release from cultured trigeminal neurons. The effect of CGRP is dose-dependent and abolished by pretreatment with CGRP receptor antagonist, CGRP(8-37). Intriguingly, CGRP-mediated BDNF release, unlike BDNF release evoked by physiological patterns of electrical stimulation, is independent of extracellular calcium. Depletion of intracellular calcium stores with thapsigargin blocks the CGRP-mediated BDNF release. Using transmission electron microscopy, our study also shows that BDNF-immunoreactivity is present in dense core vesicles of unmyelinated axons and axon terminals in the subnucleus caudalis of the spinal trigeminal nucleus, the primary central target of trigeminal nociceptors. Together, these results reveal a previously unknown role for CGRP in regulating BDNF availability, and point to BDNF as a candidate mediator of trigeminal nociceptive plasticity.

Authors+Show Affiliations

Department of Integrative Biosciences, Oregon Health and Science University, Portland, Oregon 97239, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17064360

Citation

Buldyrev, Ilya, et al. "Calcitonin Gene-related Peptide Enhances Release of Native Brain-derived Neurotrophic Factor From Trigeminal Ganglion Neurons." Journal of Neurochemistry, vol. 99, no. 5, 2006, pp. 1338-50.
Buldyrev I, Tanner NM, Hsieh HY, et al. Calcitonin gene-related peptide enhances release of native brain-derived neurotrophic factor from trigeminal ganglion neurons. J Neurochem. 2006;99(5):1338-50.
Buldyrev, I., Tanner, N. M., Hsieh, H. Y., Dodd, E. G., Nguyen, L. T., & Balkowiec, A. (2006). Calcitonin gene-related peptide enhances release of native brain-derived neurotrophic factor from trigeminal ganglion neurons. Journal of Neurochemistry, 99(5), 1338-50.
Buldyrev I, et al. Calcitonin Gene-related Peptide Enhances Release of Native Brain-derived Neurotrophic Factor From Trigeminal Ganglion Neurons. J Neurochem. 2006;99(5):1338-50. PubMed PMID: 17064360.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcitonin gene-related peptide enhances release of native brain-derived neurotrophic factor from trigeminal ganglion neurons. AU - Buldyrev,Ilya, AU - Tanner,Nathan M, AU - Hsieh,Hui-ya, AU - Dodd,Emily G, AU - Nguyen,Loi T, AU - Balkowiec,Agnieszka, Y1 - 2006/10/25/ PY - 2006/10/27/pubmed PY - 2007/1/24/medline PY - 2006/10/27/entrez SP - 1338 EP - 50 JF - Journal of neurochemistry JO - J. Neurochem. VL - 99 IS - 5 N2 - Activity-dependent plasticity in nociceptive pathways has been implicated in pathomechanisms of chronic pain syndromes. Calcitonin gene-related peptide (CGRP), which is expressed by trigeminal nociceptors, has recently been identified as a key player in the mechanism of migraine headaches. Here we show that CGRP is coexpressed with brain-derived neurotrophic factor (BDNF) in a large subset of adult rat trigeminal ganglion neurons in vivo. Using ELISA in situ, we show that CGRP (1-1000 nM) potently enhances BDNF release from cultured trigeminal neurons. The effect of CGRP is dose-dependent and abolished by pretreatment with CGRP receptor antagonist, CGRP(8-37). Intriguingly, CGRP-mediated BDNF release, unlike BDNF release evoked by physiological patterns of electrical stimulation, is independent of extracellular calcium. Depletion of intracellular calcium stores with thapsigargin blocks the CGRP-mediated BDNF release. Using transmission electron microscopy, our study also shows that BDNF-immunoreactivity is present in dense core vesicles of unmyelinated axons and axon terminals in the subnucleus caudalis of the spinal trigeminal nucleus, the primary central target of trigeminal nociceptors. Together, these results reveal a previously unknown role for CGRP in regulating BDNF availability, and point to BDNF as a candidate mediator of trigeminal nociceptive plasticity. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/17064360/Calcitonin_gene_related_peptide_enhances_release_of_native_brain_derived_neurotrophic_factor_from_trigeminal_ganglion_neurons_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04161.x DB - PRIME DP - Unbound Medicine ER -