Journal
JOURNAL OF COMPARATIVE NEUROLOGY
Volume 482, Issue 1, Pages 50-73Publisher
WILEY
DOI: 10.1002/cne.20377
Keywords
myoclonus; dystonia; dopamine; serotonin; fluorescence in situ hybridization; obsessive-compulsive disorder; panic attacks; quantum dot
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Funding
- NCI NIH HHS [R24 CA088309] Funding Source: Medline
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Myoclonus dystonia (M-D) is a hereditary movement disorder caused by a maternally imprinted gene that is often associated with psychiatric symptoms. Most cases of M-D are believed to result from mutations of the E-sarcoglycan protein. The neuroanatomical distribution Of E-sarcoglycan-like immunoreactivity in mouse was investigated by using an antiserum against the E-sarcoglycan protein. The expression Of E-sarcoglycan mRNA was studied by a sensitive fluorescence in situ hybridization (FISH) method. Immunohistochemistry and FISH revealed a wide distribution Of E-sarcoglycan protein and mRNA throughout the mouse brain. High expression levels of F-sarcoglycan mRNA and immunoreactivity were found in the mitral cell layer of the olfactory bulb, the Purkinje cell layer in cerebellum, and the monoaminergic neurons in the mouse midbrain. Immunohistochemistry revealed a similar distribution Of E-sarcoglycan protein. Double-labeling FISH showed colocalization of tyrosine hydroxylase and E-sarcoglycan mRNAs within all the midbrain dopaminergic (DAergic) cell groups. By combining FISH with fluorescence immunohistochemistry, coexpression of E-sarcoglycan mRNA and tryptophan hydroxylase immunoreactivity was found in the serotonergic (5-HTergic) neurons within the dorsal raphe nucleus. The distribution of epsilon-sarcoglycan in the mouse brain suggests that the symptom complex of M-D may be related to the effects of decreased epsilon-sarcoglycan activity on the development or function of monoaminergic neurons. (C) 2004 Wiley-Liss, Inc.
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