Hyperalgesia Induced in the Rat by the Amino-Terminal Octapeptide of Nerve Growth Factor

Nerve growth factor (NGF) in the mouse submandibular gland undergoes cleavage of its amino-terminal octapeptide when salivation is induced by epinephrine. The significance of this event is uncertain; cleaved NGF demonstrates bioactivity and no function has been attributed to the octapeptide produced...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1991-06, Vol.88 (12), p.5144-5148
Main Authors: Taiwo, Y. O., Levine, J. D., Burch, R. M., Woo, J. E., Mobley, W. C.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Bradykinin - metabolism
Carboxylic acids
Enzymes
Fundamental and applied biological sciences. Psychology
Hyperalgesia
Hyperalgesia - chemically induced
Innervation
Male
Nerve Growth Factors - pharmacology
Nerves
Neurons
Pain - chemically induced
Peptides - pharmacology
Physical trauma
Rats
Rats, Inbred Strains
Receptors
Receptors, Bradykinin
Receptors, Neurotransmitter - drug effects
Salivary glands
Sensory Thresholds - drug effects
Somesthesis and somesthetic pathways (proprioception, exteroception, nociception)
interoception
electrolocation. Sensory receptors
Vertebrates: nervous system and sense organs
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Summary:Nerve growth factor (NGF) in the mouse submandibular gland undergoes cleavage of its amino-terminal octapeptide when salivation is induced by epinephrine. The significance of this event is uncertain; cleaved NGF demonstrates bioactivity and no function has been attributed to the octapeptide produced (NGF-OP; Ser-Ser-Thr-His-Pro-Val-Phe-His). Enzyme inhibition studies indicating structural relatedness of NGF-OP and bradykinin (BK) prompted us to determine whether NGF-OP would elicit BK-like actions. We found that like BK, NGF-OP induced a decrease in mechanical nociceptive threshold (i.e., produced hyperalgesia) in the hairy skin of the rat. This effect was dose-dependent and sequence-specific; like BK it was attenuated by sympathectomy and indomethacin pretreatment. However, NGF-OP actions appeared to be distinct from those for BK in that tissue injury was required for NGF-OP to induce hyperalgesia. Furthermore, we found no evidence that NGF-OP bound to or activated BK receptors. Our data indicate that NGF-OP is a distinct mediator of hyperalgesia. We suggest that NGF-OP alters pain threshold in the injured target regions of NGF-responsive neurons.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.88.12.5144