Serotonergic modulation of a voltage-gated calcium current in parapodial swim muscle from Aplysia brasiliana.
Here we describe the effects of serotonin (5-HT) on dissociated parapodial muscle fibers from Aplysia brasiliana. 5-HT has previously been implicated as a modulatory transmitter at the parapodial neuromuscular junction. Exogenously applied or endogenously released 5-HT increases the amplitude of motoneuron-induced excitatory junctional potentials and contractions in parapodial muscle. Exogenously applied 5 microM 5-HT increases the amplitude of a voltage-gated inward calcium current in isolated muscle fibers by an average of 42% in response to a voltage step from -70 to -10 mV. The amplitude of the inward current was increased at all voltages tested, with the peak increase occurring between -30 and -20 mV. The dihydropyridine calcium channel antagonist nifedipine (10 microM) blocked this effect of 5-HT. The data indicate that 5-HT increases a previously identified calcium current in parapodial muscle fibers that is similar to the vertebrate L-type current. Although several types of K+ channels exist in these fibers, including Ca(2+)-dependent K+ channels, the results suggest that 5-HT has little effect on these currents. Parapodial muscle contractions during swimming behavior occur in response to bursts of motoneuron action potentials that produce graded muscle depolarizations that occur over a 1- to 2-s period rather than being instantaneous or rapid responses as might be produced by one or two action potentials or a brief voltage step. With the use of 1-s voltage ramps, we attempted to mimic physiological depolarization and demonstrate that 5-HT is able to increase the amplitude of the inward calcium current. The data presented in this paper provide evidence that 5-HT increases the Ca2+ current, which may be one mechanism by which 5-HT modulates muscle contractions during swim behavior.
Laurienti
P J
PJ
Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77555-1069, USA.
Blankenship
J E
JE
D000818:Animals; D001048:Aplysia / Q000502:physiology*; D001369:Axons / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D004594:Electrophysiology; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology; D009132:Muscles / Q000294:innervation / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D012701:Serotonin / Q000502:physiology*; D013550:Swimming
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D015221:Potassium Channels; D012701:Serotonin; D009543:Nifedipine