Dopamine modulates two potassium currents and inhibits the intrinsic firing properties of an identified motor neuron in a central pattern generator network

The two pyloric dilator (PD) neurons are components [along with the anterio r burster (AB) neuron] of the pacemaker group of the pyloric network in the stomatogastric ganglion of the spiny lobster Panulirus interruptus. Dopami ne (DA) modifies the motor pattern generated by the pyloric network, in par t by exciting or inhibiting different neurons. DA inhibits the PD neuron by hyperpolarizing it and reducing its rate of firing action potentials, whic h leads to a phase delay of PD relative to the electrically coupled AB and a reduction in the pyloric cycle frequency. In synaptically isolated PD neu rons, DA slows the rate of recovery to spike after hyperpolarization. The l atency from a hyperpolarizing prestep to the first action potential is incr eased, and the action potential frequency as well as the total number of ac tion potentials are decreased. When a brief (1 s) puff of DA is applied to a synaptically isolated, voltage-clamped PD neuron, a small voltage-depende nt outward current is evoked, accompanied by an increase in membrane conduc tance. These responses are occluded by the combined presence of the potassi um channel blockers 4-aminopyridine and tetraethylammonium. In voltage-clam ped PD neurons, DA enhances the maximal conductance of a voltage-sensitive transient potassium current (I-A) and shifts its V-act to more negative pot entials without affecting its V-inact. This enlarges the "window current" b etween the voltage activation and inactivation curves, increasing the tonic ally active I-A near the resting potential and causing the cell to hyperpol arize. Thus DA's effect is to enhance both the transient and resting K+ cur rents by modulating the same channels. In addition, DA enhances the amplitu de of a calcium-dependent potassium current (I-O(Ca)), but has no effect on a sustained potassium current (I-K(V)) These results suggest that DA hyper polarizes and phase delays the activity of the PD neurons at least in part by modulating their intrinsic postinhibitory recovery properties. This modu lation appears to be mediated in part by an increase of I-A and I-O(Ca). I- A appears to be a common target of DA action in the pyloric network, but it can be enhanced or decreased in different ways by DA in different neurons.