Functions of primary afferents and responses of extracellular K+ during spinal epileptiform seizures.

Published

Journal Article

Paroxysmal activity in ventral roots induced by penicillin in decapitate cat spinal cords is associated with waves of depolarization of primary afferent fiber terminals. These paroxysmal depolarizations can be detected as spontaneously occurring negative dorsal root potentials (DRPs) and are associated with antidromic discharge of nerve impulses in dorsal root fibers; they can also be detected by testing the excitability of afferent nerve terminals by focal stimulation. Negative DRPs evoked by afferent nerve volleys are altered in waveform but not in amplitude during seizures induced by penicillin, although they are blocked by the administration of picrotoxin. While blocking afferent-evoked DRPs, picrotoxin does not interfere with paroxysmal DRP'S, INDICATING DIFFERENCES IN THE GENERATION OF THE Two phenomena, which nevertheless have some link in common, for the paroxysmal waves occlude the evoked DRP. Such occlusion would appear as blockade, if DRPs were recorded by condenser-coupled amplifiers. In the presence of pentobarbital penicillin suppresses evoked DRPs, but under such circumstances seizure activity is not observed. Extracellular potassium activity within spinal gray matter transiently increases during seizure activity. Such increments of potassium activity are maximal in the ventral horns. This and several other observations suggest that in decapitate spinal cords systemically administered penicillin induces seizures which originate in the ventral gray matter. Accumulation of excess potassium may be the cause of paroxysmal depolarization of afferent nerve terminals. Excess potassium while not playing a principal role in initiating seizures, may influence the course of seizures by depolarizing afferent terminals. Such depolarization probably enhances tonic background release of transmitter substance, may modify the effect of synaptic input, and may favor synchronization of waves of neural excitability through extrasynaptic mechanisms.

Full Text

Duke Authors

Cited Authors

  • Lothman, EW; Somjen, GG

Published Date

  • September 1, 1976

Published In

Volume / Issue

  • 41 / 3

Start / End Page

  • 253 - 267

PubMed ID

  • 60213

Pubmed Central ID

  • 60213

International Standard Serial Number (ISSN)

  • 0013-4694

Digital Object Identifier (DOI)

  • 10.1016/0013-4694(76)90118-8

Language

  • eng

Conference Location

  • Ireland