Abstract
We have described that NIL Lewis rats develop mild signs of acute EAE with no changes in the HPA axis activity. Lewis and Wistar rats develop EAE, but differences in the HPA axis response to EAE exist between them. This suggests a different strain‐specific role of corticosterone (CO) in the immunoregulation of the EAE. Here we study the effects of CO and neurohypophyseal (NH) hormones deficiency (NIL) on the EAE. Rats from both strains were sham operated (SHAM) or NIL. Three weeks after surgeries rats were immunized with an encephalitogenic emulsion, and clinical course of EAE registered before and after ADX (performed at 27 day post‐immunization (DPI)). SHAM animals of both strains developed similar transient paralytic scores of EAE (10–20 DPI). In both strains, NIL induced decreased scores of the EAE. In Wistar SHAM ADX and NIL ADX groups no relapses of EAE occurred, whereas in Lewis SHAM ADX and NIL ADX groups a prompt and worse relapse of the EAE occurred, similar to the observed in the acute paralysis.Conclusions: 1) In NIL Wistar and Lewis groups, decreased severity of the EAE is under the NH hormones control, 2) In Wistar rats CO‐independent mechanisms protect against the EAE relapses, 3) In Lewis rats CO is required to protect against the EAE relapses, 4) Although NH hormones and CO participate in the immunopathology of the EAE it seems that they work through different mechanisms.
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