A single GTP-binding protein regulates K+-channels coupled with dopamine, histamine and acetylcholine receptors

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Abstract
Recently, a GTP-binding protein sensitive to islet activating protein (IAP) has been suggested to be important in producing K+-currents when the muscarinic receptor of the atrial muscle is activated by acetylcholine (ACh)1–3. Here we confirm the blocking effects of IAP and GTPγS (a nonhydrolysable analogue of GTP) on the ACh-induced Recurrent recorded from the ganglion cells of the sea slug Aplysia and compare their effects on histamine (HA)-induced and dopamine (DA)-induced K+-currents. Intracellular injections of IAP irreversibly and selectively block the openings of K+-channels activated by either ACh, HA, or DA without affecting the resting potential or conductance states of the membranes. Intracellular application of GTPγS alone caused extremely slow, irreversible opening of K+-channels; however, repetitive receptor activations significantly increase the rate of the GTPγS effect. These results strongly suggest that a GTP-binding protein such as Gi regulates the opening of K+-channels coupled with these receptors.