Myelinating Schwann cells express the gap junction protein, connexin (Cx)32
, which is present at the nodes of Ranvier and Schmidt-Lantermann incisures
(Bergoffen et al, [1993] Science (Wash,) 262:2039-2042), Following periphe
ral nerve injury, other members of the connexin gene family are also expres
sed (Chandross et al, [1996a] Mel. Cell. Neurosci, 7:501-518), This study s
urveys the connexin(s) expressed by rat sciatic nerve, cultured Schwann cel
ls, and a mouse Schwannoma (TR6 Eel) cell line. Reverse transcriptase-polym
erase chain reaction (RT-PCR) amplification revealed a constitutive express
ion of mRNA encoding Cx32 and 43 but not Cx26, 37, 40, 45, and 46 in sciati
c nerve. Mitogenic stimulation of cultured Schwann cells expressing Cx32 al
so resulted in the appearance of Cx43 mRNA, Schwannoma cells expressed excl
usively Cx43 mRNA, These results were confirmed by Northern blot analysis.
Functional gap junctions in cultured Schwann and Schwannoma cells were show
n by analysis of the intercellular transfer of Lucifer yellow, although the
coupling between primary Schwann cells was weak or undetectable. Treatment
of primary Schwann cells with mitogens resulted in extensive dye coupling.
An immunohistochemical study of adult sciatic nerve sections demonstrated
Cx32 immunoreactivity at the nodes of Ranvier and in Schwann cell bodies. L
ower intensity staining of Cx43 along the myelin sheath and Schwann cell bo
dies was also observed. Indirect immunofluorescent studies of Schwann cells
treated with mitogens showed characteristic punctate cell surface staining
of Cx43; Cx32 staining was detected mainly intracellularly. These results
lead to the conclusion that in addition to the expression of Cx32 by normal
adult sciatic nerve, low amounts of Cx43 protein are also present. The imp
lications of the expression of two connexins by Schwann cells in Charcot-Ma
rie-Tooth X-linked disease, a demyelinating peripheral neuropathy, are disc
ussed. J, Neurosci, Res. 57:166-175, 1999, (C) 1999 Wiley-Liss, Inc.