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The most characteristic property of microglia is their swift activation in response to neuronal stress and their capacity for site-directed phagocytosis. The transformation of microglia into intrinsic brain macrophages appears to be under strict control and takes place if neuronal and/or terminal degeneration occurs in response to nerve lesion. The differentiation of microglia into brain macrophages is accompanied by the release of several secretory products, e.g., proteinases, cytokines, reactive oxygen intermediates, and reactive nitrogen intermediates. Interference with the microglial activation or the productions of cytotoxic metabolites by microglia may thus offer new therapeutic opportunities for the prevention of neuronal cell death in CNS disease.

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factors and/or extracellular signalling molecules different from those controlling the astrocyte properties in the fully developed brain. The expression of voltage-dependent calcium (Ca 2+) currents and inward-rectifying potassium (K +) currents can be triggered by the co-cultivation of astrocytes with neurons [4,6]. Ca 2÷ currents were also recorded in pure astrocyte cultures after a short time elevation of the intracellular content of cAMP [7,8]. Long-term treatment with dibutyryl-cyclic-AMP (dBcAMP), a permeable analog of cAMP, of astrocyte cultures has been reported to induce morphological and biochemical changes which have also been taken as an indicator for astrocyte differentiation [9 16]. However, little is known whether in astrocytes this goes along with a parallel modification of the electric membrane properties [17].We investigated this issue in patch-clamp experiments performed on rat cultured cortical astrocytes which had been incubated for 1 3 weeks with 250HM dBcAMP. The results indicate that the prolonged strengthening of the cAMP signalling causes, in conjunction with morphological/biochemical signs of astrocyte differentiation, the new expression of kinetically and pharmacologically distinct inwardly rectifying K + and CI-conductances which may be implicated in the astrocyte function of extracellular K + buffering.