Role of Potassium in Anomalous Motor Neuron Firing

Stephens, Philip

Abstract

The proposed study will examine why certain neurons change their firing patterns. The study will use two crustacean motor axons, the fast (FBE) and slow (SBE) motor axons to the limb bender muscle. When warmed or bathed in saline containing ethanol, FBE changes from single to bursts of spikes in response to a brief electrical shock; the SBE only fires in single spikes. The FBE spike is followed by a depolarizing afterpotential (DAP), which produces the extra spikes. The study will test the theory that the DAP is produced by potassium ions that leave the axon during the spike, accumulate in a small extracellular space and depolarize the potassium equilibrium potential (Ek) above resting (Em). The study will be conducted in two sections: 1. Microelectrodes will be used to measure intracellular potassium concentration and calculate Ek. The theory maintains that, at rest, Ek-Em will be less in the FBE axon so that after the spike it will be at a more depolarized level than in SBE - producing a larger DAP in FBE. The effects of ethanol and temperature on Ek will be examined. 2. Voltage clamp techniques will be applied to the axons to determine whether a fast (""""""""A"""""""") potassium current is present. The effects of temperature and ethanol on the amplitude and time course of the A-current will be determined, to explain how warming and ethanol increase DAP amplitude, while the spike gets smaller and briefer. The FBE axon has features similar to those seen in some mammalian neurons: under certain conditions the neurons produce additional spikes and fire in anomalous, epileptic bursts. Crustacean axons hold many advantages over mammalian neurons, since their large diameters permit the use of microelectrode techniques. Moreover, a second (SBE) axon does not produce additional spikes and gives a unique opportunity to compare the properties of two axons, and study the mechanisms that underlie the production of anomalous spike bursts.