Article Review – Nerve Growth Factors (NGF)

Article Review

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The article under review is titled, ‘Nerve growth factors contribute to the generation of inflammatory sensory hypersensitivity’, by Woolf et al. (1994). The review seeks to explain the background of the study, the main findings of the study, and the contribution each has made to the establishment of peripheral sensitization as a major mechanism in pain neurobiology.

In their article, Woolf et al. (1994) have endevoured to explore the role of nerve growth factor (NGF) in inflammatory pain. Inducing inflammatory pain using Freund’s adjuvant causes local sensory hypersensitivity and up-regulates the neuropeptide substance P and calcitonin gene-related peptide in the major efferent neurons feeding the inflamed tissue. In addition, inflammation increases the levels of nerve growth factor in the skin. Injecting of anti-NGF neutralizing antibodies hinders behavioural sensitivity and the increase of neuropepotides as well as the expression of the initial early gene c-fos in dorsal horn neurons without changing swelling and erythema – reddening of the skin.

This article reports the findings of a study to test the role NGF plays in the pathogenesis of inflammation. The authors studied the effects of administering anti-NGF antibodies on the sensitivity induced by injection of an exogenous Freund’s adjuvant (CFA) in a hind paw of adult rats. The injection of the CFA in the right spot induced erythema and oedema within 6 hours that was localised, lasting for more than 15 days. This effect was accompanied by an increase in mechanical and thermal hypersensitivity that was highest at the injection site and also at the contralateral regions. Administering a specific dose of anti-NGF an hour before the injection of CFA and 24 hours later alleviated the results of the CFA-related hypersensitivity in the contralateral hind paw besides the ipsi. However, the effects of the anti-NGF did not have any statistically significant effects on erythema or oedema. Nevertheless, the decrease in thermal and mechanical sensitivity triggered by the anti-NGF began about six hours after the administration of CFA lasted for about 48 hours, and remained relatively high until after five days when it started to fade away.

The anti-NGF and IgG-enriched portions decreased sensitivity, but the sheep serum or their IgG forms did not have any effect on sensitivity. Importantly, the results of the study also showed that running anti-NGF through an affinity column reduced its hypersensitivity. Anti-NGF injection without CFA lesion had a negligible effect on mechanical or thermal sensitivity when assessed 48 hours after the initial 2 injections given at 24-hour intervals. Intraplantar injection of the turpentine oil had synergistic effects on the anti-NGF serum administration.

Injecting anti-NGF five days following CFA injection alleviated thermal sensitivity after a shorter interval (3 hours) than mechanical sensitivity (13) hours. These results show that continuing production of NGF contributes to the maintenance of persistent changes in sensitivity. The findings of the study also support the past results that CFA inflammation increases NGF levels in peripheral nerves, which corresponds to the evidence of inflamed skin.

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