Axonal sprouting and synaptogenesis in temporal lobe epilepsy: possible pathogenetic and therapeutic roles of neurite growth inhibitory factors

Seizure. 1995 Dec;4(4):249-58. doi: 10.1016/s1059-1311(95)80001-8.

Abstract

Axonal sprouting and synaptic reorganization within the temporal lobe following neuronal injury have been implicated in the pathogenesis of temporal lobe epilepsy (TLE). The molecular species responsible for these structural changes have yet to be fully defined. The recent characterization of molecules whose normal function within the nervous system is to inhibit neurite outgrowth and synaptogenesis prompts the suggestion that a diminution or loss of such molecules might be of relevance to the pathogenesis of TLE. If so, the possibility of developing a novel therapeutic approach to TLE, distinct from currently available symptomatic therapies, to arrest the pathogenetic processes is also raised.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / physiopathology
  • Animals
  • Axons* / drug effects
  • Axons* / physiology
  • Brain / drug effects
  • Brain / physiopathology
  • Epilepsy, Temporal Lobe / chemically induced
  • Epilepsy, Temporal Lobe / drug therapy*
  • Epilepsy, Temporal Lobe / physiopathology*
  • Humans
  • Kainic Acid / adverse effects
  • Kainic Acid / pharmacology
  • Nerve Growth Factors / adverse effects
  • Nerve Growth Factors / pharmacology
  • Nerve Growth Factors / therapeutic use*
  • Neuronal Plasticity
  • Rats
  • Receptors, GABA / drug effects
  • Receptors, N-Methyl-D-Aspartate / drug effects
  • Synapses* / drug effects
  • Synapses* / physiology

Substances

  • Nerve Growth Factors
  • Receptors, GABA
  • Receptors, N-Methyl-D-Aspartate
  • Kainic Acid