Neurochem Int. 2004 Aug-Sep;45(2-3):243-50
Iacobas DA, Scemes E, Spray DC.
Department of Neuroscience, Albert Einstein College of Medicine, Kennedy Center, Room 915C, 1300 Morris Park Ave, Bronx, NY 10461, USA.
Connexin43 (Cx43) is the principal gap junction protein between astrocytes in the neonatal brain and also interconnects neural precursor cells during CNS development.
In an attempt to understand global effects of expression of the Cx43 gap junction gene on development and function of the nervous system, we have compared gene expression patterns in cultured astrocytes and brains from wildtype mice with those in which Cx43 is deleted as well as in spinal cords of experimental autoimmune encepahlomyelitis (EAE) mice.
One surprising result obtained from high densitity mouse cDNA studies was the large number of genes that were statistically altered in mice with decreased expression of Cx43.
These altered genes encode proteins with a wide range of functions within cells, and thus deletion of normal gap junction expression appears to result in globally altered glial functions in addition to disruption of intercellular communication.
Here we discuss those results in the context of the strategies and data analysis paradigms that we are using in such studies.