JACKLET, J W; GRIZZAFFI, J; TIEMAN, D G; University at Albany; University at Albany; University at Albany: Serotonin Induces Tonic and Spike-burst Activity in Metacerebral Neurons of Aplysia.

Serotonin is an important neuromodulator of Aplysia neurons. It increases excitability and broadens action potentials resulting in enhanced transmitter release from sensory neurons. Its release from serotonergic metacerebral cells (MCCs) produces excitatory modulation of feeding circuit neurons and buccal muscles. We find that 10 uM serotonin is sufficient to increase the membrane resistance and depolarize MCCs. The normally silent neurons then produce tonic spike activity, which gives way to spike-burst activity in a few minutes. We examined the membrane ionic current changes during serotonin treatment in the -100 to -30 mV range and found small steady-state inward currents near the resting potential of -60 mV but larger inward shifts in current between -45 and -30 mV and between -75 and -100 mV. 8-Br-cAMP produced a similar result. Transient calcium currents (blocked by 10 mM cobalt) in the -40 to -30 mV range are enhanced by serotonin. The currents in the -75 to -100 mV range are blocked by 10 mM barium or cesium and likely potassium currents. It appears that initially a potassium current (S current) is blocked by serotonin or cAMP, as it is in sensory neurons, to cause the depolarization and enhanced sodium and calcium currents that contribute to the spiking. The periodic hyperpolarization during serotonin induced bursting may be initiated by activation of a calcium dependent potassium current and enhanced by voltage dependent potassium currents. Additionally, the presence of depolarizing serotonin receptors on MCC suggests that serotonin released by these neurons at their synaptic terminals may augment their transmitter release.