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β‐Adrenergic Modulation of Glial Inwardly Rectifying Potassium Channels

Abstract: Cultured spinal cord astrocytes (2–13 days in vitro) express several different potassium current types, including delayed rectifier, transient A‐type, and inward rectifier (Kir) K+ currents. Of these, Kir is believed to be of critical importance in the modulation of extracellular [K+] in the CNS. Using the whole‐cell patch‐clamp technique, we analyzed modulation of Kir currents by β‐adrenergic receptor activation. The selective β‐adrenergic agonist isoproterenol (1–100 µM) and epinephrine (1–100 µM) each reduced peak Kir current amplitudes to 52.7 ± 12.5 and 63.6 ± 7.0%, respectively, at 100 µM. Forskolin (KD of ∼25 µM), an activator of adenylate cyclase (AC), and dibutyryl‐cyclic AMP (1 mM), a membrane‐permeable analogue of cyclic AMP (cAMP), were each used to increase [cAMP]i, the product of AC, and resulted in similar reductions of Kir currents. By contrast, 1,9‐dideoxyforskolin (1–50 µM), a forskolin analogue that does not activate AC, did not affect Kir currents, indicating that AC activity is a required element for Kir modulation. Three inhibitors of PKA—Rp‐adenosine 3′,5′‐cyclic monophosphothioate, H‐7, and adenosine 3′,5′‐cyclic monophosphate‐dependent protein kinase inhibitor—failed to inhibit Kir current reduction by β‐adrenergic agonists. These results indicate that β‐adrenergic receptor ligands can modulate Kir currents and suggest that this modulation involves activation of AC but not protein kinase A. Such modulation may provide a mechanism by which neurons can modulate glial Kir currents and thereby may affect glial K+“spatial buffering” in the CNS.