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G J Bennett

Publications and source records attributed to G J Bennett.

77 records · Page 5Linked to original sources
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Dynorphin increases in the dorsal spinal cord in rats with a painful peripheral neuropathy.

It is known that painful tissue injury evokes an increase in dynorphin in spinal neurons. It is not known, however, whether dynorphinergic systems respond similarly to the pain that accompanies peripheral neuropathy. Radioimmunoassays and immunocytochemistry were used to evaluate changes in dynorphin A(1-8) in the spinal cord of rats with a painful peripheral neuropathy. The neuropathy is the result of a constriction injury that is created by tying loose ligatures around the common sciatic nerve. Signs of abnormal pain sensations, hyperalgesia, allodynia (pain after normally innocuous stimuli), and spontaneous pain (or dysesthesia), are first detected 2-5 days after injury, reach peak severity in about 10 days, and persist for 2-3 months (Bennett, G. J.; Xie, Y.-K. Pain 33:87-107; 1988). Dynorphin increased by 5 days in cells in laminae I-II and V-VII in the lumbar spinal cord ipsilateral to the injury. This increase, maximal at 10 days (262%), was still present 20 days after the injury but was now seen only in neurons in the deep laminae (V-VII). Thus, the spinal dynorphinergic system appears to respond to neuropathic pain. Furthermore, our results suggest that dynorphinergic cells in the superficial and deep laminae may have different roles in nociception.

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Quantitative autoradiographic analysis of [125I]-human CGRP binding sites in the dorsal horn of rat following chronic constriction injury or dorsal rhizotomy.

Quantitative receptor autoradiography was used to examine the binding of [125I]-human CGRP in the dorsal horn of the L4 spinal segment of rats with a chronic constriction injury (CCI) of the sciatic nerve or unilateral dorsal rhizotomies of spinal segments L1-L6. At the times selected for study, we found no change in the amount of CGRP binding in any areas examined following CCI. In contrast, our results showed a temporally related increase in the amount of CGRP binding in areas within laminae I-II and in lateral lamina V of the dorsal horn ipsilateral to the rhizotomies. These results indicate that CGRP binding sites are regulated, most likely, by changes in the release of CGRP. Further, our results suggest that the release of CGRP from primary afferent neurons is unchanged in animals with a CCI.

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Effect of local methylprednisolone on pain in a nerve injury model. A pilot study.

BACKGROUND AND OBJECTIVES: Local injections of corticosteroids are frequently used in the treatment of regional pain. The rationale for this is not very clear, since an inflammatory cause of pain is rarely evident. There are few data on the effect of corticosteroids on nociception in experimental animals. However, corticosteroids have been found to suppress ectopic discharges from experimental neuromas and to have a short-lasting suppressive effect on transmission in normal C-fibers. In this study the influence of a locally applied depot form of a corticosteroid on neuropathic pain was investigated in a rat model. METHODS: Peripheral mononeuropathy was induced with a chronic constriction injury to the left sciatic nerve. This procedure has previously been shown to produce various signs of disturbed sensibility, including heat hyperalgesia, mechanical allodynia, and mechanical hyperalgesia, indicating that a neuropathic pain-like condition has developed. The occurrence of neuropathic pain in these animals was confirmed with behavioral testing after 9 days. The site of injury was then reexposed and treated locally with either a depot form of a corticosteroid (methylprednisolone) or saline. The animals were then tested for another 11 days. RESULTS: The heat hyperalgesia and mechano-allodynia but not the mechano-hyperalgesia were depressed in the animals receiving the corticosteroid but not in those treated with saline. The effect remained during the whole 11-day test period. CONCLUSIONS: It is hypothesized that the corticosteroid acts by suppression of ectopic neural discharges from the injured nerve fibers.

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