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We performed patch-clamp recordings on acutely isolated dendritic segments and cell somata of rat neocortical pyramidal neurons to determine and compare the relative density of G protein-activated K+ (GIRK) currents in the two cellular compartments.
Hyperpolarizing voltage ramps and elevation of extracellular K+ concentration to 40 mM served to identify inwardly rectifying K+ currents. Near-saturating concentrations of adenosine (100 µM), baclofen (20 µM) and serotonin (20 µM) all produced robust GIRK currents in cell somata as well as in dendritic segments that were completely abolished by Ba2+ (200 µM). In addition to agonist-activated GIRK currents, both somata and dendrites displayed a constitutive Ba2+-sensitive inward rectification.
In order to compare the relative strengths of GIRK current responses in the two compartments, GIRK conductance was normalized to surface area. In contrast to intrinsic, G protein-independent inward rectification, which was comparable in size in the two compartments, all three agonists evoked significantly larger GIRK conductances in dendrites than in somata.
Our data suggest that several neurotransmitters might employ GIRK currents as a tool to directly modulate the electrical properties of dendrites. In concert with voltage-dependent K+ currents and the hyperpolarization-activated cation current (Ih) of the dendrite, GIRK currents should dampen dendritic excitability and thus influence various aspects of dendritic signal integration.
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