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APOPTOSIS IN AN EXCITOTOXIC MODEL OF POST-TRAUMATIC SYRINGOMYELIA



Abstract

INTRODUCTION: Apoptosis has been observed following experimental contusive and transective spinal cord injury, but it is not known whether this is related to secondary excitotoxic injury or other factors. This study examines apoptosis after a purely excitotoxic injury and the relationship between apoptosis and syrinx formation.

METHODS: Twenty-four male Sprague-Dawley rats were divided into six groups. Twenty rats received four 0.5 μL injections of 24 mg/mL quisqualic acid and 1% Evans blue between the rostral C8 and caudal T1 level. Ten microliters of 250 mg/mL kaolin were then injected into the subarachnoid space. Animals were sacrificed at 1, 5, 10, 20 and 50 days following the injections. There were four control animals. Spinal cord tissue was frozen and sectioned, and damaged DNA was detected immunohistochemically by using anti-single-stranded DNA monoclonal antibody. The area and density of single strand DNA were semi-quantitated.

RESULTS: No significantly damaged DNA was found in the 1 day group. Light staining of single-stranded DNA was observed at C6, C7, T1 and T2 levels in 30% of the section area in the 5 and 10 day groups. Moderate staining of damaged DNA occurred at C7 and T1 levels in 25–30% of the section area at 20 day group. Syrinxes formed in this group. Heavy staining and larger syrinxes were noted in the 50 day group.

DISCUSSION: Apoptosis increased with time after excitotoxic injury. These findings suggest that apoptosis may play a pivotal role in syrinx pathogenesis.

These abstracts were prepared by Dr Robert J. Moore. Correspondence should be addressed to him at Spine Society of Australia, Institute of Medical and Veterinary Science, The Adelaide Centre for Spinal Research, Frome Road, Adelaide, South Australia 5000.