From: Kofi on

Exp Biol Med (Maywood). 2009 Nov;234(11):1383-92.

Endogenous opioids regulate expression of experimental autoimmune
encephalomyelitis: a new paradigm for the treatment of multiple
sclerosis.
Zagon IS, Rahn KA, Turel AP, McLaughlin PJ.
Department of Neural and Behavioral Sciences, H109, The Milton S.
Hershey Medical Center, 500 University Drive, Room C3729, Hershey, PA
17033, USA.

Preclinical investigations utilizing murine experimental auto-immune
encephalomyelitis (EAE), as well as clinical observations in patients
with multiple sclerosis (MS), may suggest alteration of endogenous
opioid systems in MS. In this study we used the opioid antagonist
naltrexone (NTX) to invoke a continuous (High Dose NTX, HDN) or
intermittent (Low Dose NTX, LDN) opioid receptor blockade in order to
elucidate the role of native opioid peptides in EAE. A mouse model of
myelin oligodendrocyte glycoprotein (MOG)-induced EAE was employed in
conjunction with daily treatment of LDN (0.1 mg/kg, NTX), HDN (10 mg/kg
NTX), or vehicle (saline). No differences in neurological status
(incidence, severity, disease index), or neuropathological assessment
(activated astrocytes, demyelination, neuronal injury), were noted
between MOG-induced mice receiving HDN or vehicle. Over 33% of the
MOG-treated animals receiving LDN did not exhibit behavioral signs of
disease, and the severity and disease index of the LDN-treated mice were
markedly reduced from cohorts injected with vehicle. Although all LDN
animals demonstrated neuropathological signs of EAE, LDN-treated mice
without behavioral signs of disease had markedly lower levels of
activated astrocytes and demyelination than LDN- or vehicle-treated
animals with disease. These results imply that endogenous opioids,
evoked by treatment with LDN and acting in the rebound period from drug
exposure, are inhibitory to the onset and progression of EAE, and
suggest that clinical studies of LDN are merited in MS and possibly in
other autoimmune disorders.

Publication Types:
* Research Support, Non-U.S. Gov't

PMID: 19855075