Astrocyte gap junctions and glutamate-induced neurotoxicity

Abstract

In brain, gap junctions are widely expressed in various cell types including neurons and glial cells. They are present between neurons at electrical synapses (Bennett, 1977) and provide the intercellular pathway for astrocytic networks (Giaume and McCarthy, 1996). We have recently reviewed the expression of gap junctions in the central nervous system and discussed their physiopathological relevance in several brain dysfunctions (Rouach et al., 2002b). In the present chapter, we focus on the expression and function of connexins (Cxs) in a major glial cell population, the astrocytes, that outnumber neurons and make up about 50% of human brain volume (Tower and Young, 1973). Data indicating that astrocytic connexins represent an identified target of neuroglial and glial-glial interactions and that changes in their properties and/or their pattern of expression may be relevant in physiopathological situations are described. With that objective, we concentrate on the role of glutamate, which plays a key role in neurotoxic processes, and as a working hypothesis we discuss the potential contribution of astrocyte gap junctional communication (GJC) in the homeostasis of this excitatory amino acid.