Sustained depolarizing potentials in reticulospinal axons during evoked seizure activity in lamprey spinal cord.

Abstract

1. Intracellular recordings were made from lamprey reticulospinal axons (Müller axons) during seizures evoked by electrical stimulation of the isolated spinal cord in saline containing either 0 Cl or 1 mM picrotoxin. The seizures had tonic and clonic-phases similar to ictal seizures in mammalian brain. 2. During seizures Müller axons were depolarized by 10-15 mV. These seizure-depolarizations were not due to any direct effect of the evoking stimulus on the Müller axons themselves nor were they initiated by an accumulation or extracellular potassium. 3. A decrease in axonal input resistance occurred during a seizure-depolarization. Also, the amplitude of a seizure-depolarization was decreased by depolarizing the axon 5-15 mV with injected current. Further, hyperpolarizing the axon increased the amplitude of the seizure-depolarization, but the growth flattened out beyond 30-40 mV of hyperpolarization. The decrease in input resistance during the seizure-depolarization and the dependence of the response amplitude on axonal membrane potential suggested that the seizure-depolarization was an excitatory synaptic potential. However, the failure of the seizure-depolarization amplitude to continue to grow at membrane potentials greater than 30 mV negative to the resting potential was not consistent with this interpretation. 4. A synaptic conductance change as the cause of the seizure-depolarization was ruled out by setting the axonal membrane potential at different levels with injected current and monitoring the input resistance of the axon before and during seizure-depolarizations. It was found that no change in input resistance occurred during the seizure-depolarization when the axon was hyperpolarized more than approximately 30 mV, the same potential at which the growth in the response amplitude ceased. From analysis of these data and the passive current-voltage properties of Müller axons it is concluded that the seizure-depolarization is not a chemical synaptic potential, but rather the result of the passive injection of depolarizing current into the axons. 5. The source of the depolarizing current which flows into Müller axons during seizures is probably paroxysmal action-potential activity in spinal motoneurons and interneurons, many of which are electrically coupled to Müller axons.