Selected Publication:
Amann, R; Schuligoi, R; Herzeg, G; Donnerer, J.
Intraplantar injection of nerve growth factor into the rat hind paw: local edema and effects on thermal nociceptive threshold.
Pain. 1996; 64(2):323-329
Doi: 10.1016%2F0304-3959%2895%2900120-4
Web of Science
PubMed
FullText
FullText_MUG
Google Scholar
- Leading authors Med Uni Graz
-
Amann Rainer
- Co-authors Med Uni Graz
-
Donnerer Josef
-
Schuligoi Rufina
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Nerve growth factor (NGF) is known to produce hyperalgesia as well as to stimulate synthesis of neuropeptides in dorsal root ganglia (DRG). In the present study, we wanted to determine the effects of local NGF administration and assess to which extent mast cell-dependent factors are mediating NGF responses. Rats received 1 daily unilateral intraplantar injection for 3 days. Local edema (days 1-3), changes in thermal nociceptive threshold (days 1-4), and the content of calcitonin gene-related peptide (CGRP) and substance P (SP) in the sciatic nerve (day 4), were determined. NGF injection caused edema which was absent in rats pretreated with compound 48/80 as well as in rats treated neonatally with capsaicin ('capsaicin denervation'). NGF-induced edema was not reduced by the neurokinin-1 receptor antagonist SR140333, but attenuated by the CGRP receptor antagonist CGRP[8-37]. On each day, NGF injection caused a decrease in thermal nociceptive threshold which lasted for less than 3 h. Capsaicin denervation, but not treatment with indomethacin, abolished NGF-induced thermal hyperalgesia. Treatment with compound 48/80 attenuated hyperalgesia produced by the first, but not by subsequent, NGF injections. On day 4, 24 h after the last of 3 NGF injections, thermal nociceptive threshold was not different from control values, but at that time, CGRP and SP were elevated in the sciatic nerve. We suggest therefore that NGF-induced local edema was caused by mast cell-derived vasoactive compounds which act together with afferent neuron-derived CGRP to increase vascular permeability. NGF-induced thermal hyperalgesia most likely was caused by an increased sensitivity of peripheral endings of capsaicin sensitive afferents. This effect of NGF was not mediated by products of the cyclooxygenase pathway, and was also observed in mast cell-depleted rats.
- Find related publications in this database (using NLM MeSH Indexing)
-
Animals -
-
Calcitonin Gene-Related Peptide - metabolism
-
Capsaicin - pharmacology
-
Cyclooxygenase Inhibitors - pharmacology
-
Denervation - pharmacology
-
Edema - chemically induced
-
Foot - pathology
-
Histamine - metabolism
-
Injections - metabolism
-
Male - metabolism
-
Mast Cells - drug effects
-
Nerve Growth Factors - administration and dosage
-
Neurons, Afferent - drug effects
-
Pain Threshold - drug effects
-
Rats - drug effects
-
Rats, Sprague-Dawley - drug effects
-
Sciatic Nerve - drug effects
-
Substance P - metabolism
- Find related publications in this database (Keywords)
-
Nerve Growth Factor
-
Thermal Hyperalgesia
-
Compound 48/80
-
Capsaicin
-
Neuropeptide