The Coxackievirus and Adenovirus receptor (CAR) was originally identifi ed as a cell surface protein enabling both viruses to interact with cells. Besides this pathological role as a virus receptor, the physiological function of CAR in the CNS is largely unknown. CAR is a member of the Ig superfamily composed of two Ig-like domains, a transmembrane stretch and a cytoplasmic segment. CAR is expressed early in development on neurons and becomes restricted to synapse-rich layers at more advanced stages. Application of the fi ber knob of the adenovirus, which binds to CAR, resulted in longer neurites in comparison to the untreated cell cultures. Furthermore, the formation of cell aggregates was reduced by the fi ber knob. By using whole-cell patch clamp technique we analyzed the effect of the fi ber knob on passive membrane properties and synaptic activity. The fi ber knob reduces the membrane resistance (Rm) of cultured neurons. Consistently, in CAR defi cient neurons Rm was signifi cantly higher compared to wild type neurons, and application of fi ber knob had no effect on Rm on CARdefi cient neurons. Thus, CAR may infl uence Rm via membrane proteins with a membrane conductance (e.g. ion channels, gap junction). Our model is, that CAR defi cient neurons may not express or express some not functional ion channel or transport proteins in the membrane. On the other side, binding of the fi ber knob to CAR might induce activation – opening of such transport protein.
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