Dopamine receptor activation can reduce voltage-gated Na+ current by modulating both entry into and recovery from inactivation.
We tested whether dopamine receptor activation modulates the voltage-gated Na+ current of goldfish retinal ganglion cells, using a fast voltage-clamp amplifier, perforated-patch whole cell mode, and a physiological extracellular Na+ concentration. As found in other cells, activators of D1-type dopamine receptors and of protein kinase A reduced the amplitude of current activated by depolarizations from resting potential without altering the current kinetics or activation range. However, D1-type dopamine receptor activation also accelerated the rate of entry into inactivation during subthreshold depolarizations and slowed the rate of recovery from inactivation after single, brief depolarizations. Our results provide the first evidence in any preparation that D1-type receptor activation can produce both of these latter effects.
Section of Neurobiology, Physiology, and Behavior, University of California, One Shields Ave., Davis, CA 95616-8519, USA.
Yuki
Y
Hayashida
Andrew T
AT
Ishida
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000818:Animals; D006054:Goldfish; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D011954:Receptors, Dopamine / Q000502:physiology*; D017447:Receptors, Dopamine D1 / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000502:physiology*; D015222:Sodium Channels / Q000502:physiology*
D011954:Receptors, Dopamine; D017447:Receptors, Dopamine D1; D015222:Sodium Channels; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine