Abstract
Experimental allergic encephalomyelitis (EAE) is an animal model for the human neurological disease multiple sclerosis (MS). Upon immunization with guinea pig spinal cord under a low dose of Cyclosporin A, male Lewis rats develop a severe chronic (relapsing) course of EAE (CR-EAE). By contrast, female Lewis rats develop a more mitigated course of EAE: only half of the female rats develop relapses. To further analyze factors determining this sexual dimorphism in the course of EAE, in the present study male and female Lewis rats were gonadectomized before induction of CR-EAE. Now both male and female rats all developed a severe chronic course of EAE, showing extensive pathological changes in the CNS. In the female sham-gonadectomy (control) group only one third of the rats developed relapses. These female rats only showed mild pathological changes in the CNS. In the male sham-gonadectomy (control) group all rats developed relapses of EAE and showed extensive pathological changes in the CNS. From these data we conclude that the presence of the ovaries (partially) protects female rats against relapses of EAE and CNS injury. Presence or absence of the testes apparently makes no difference on the course of EAE. We propose that sex hormones produced in the ovaries protect female rats against relapses of EAE and underlying CNS injury.
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