Survey of ALS-associated factors potentially promoting Ca2+ overload of motor neurons

Amyotroph Lateral Scler. 2007 Oct;8(5):260-5. doi: 10.1080/17482960701523124.


The deleterious consequences of Ca(2+) overload are thought to be a probable cause of motoneuronal death in ALS, although the overloading mechanism is currently unclear. In this paper some ALS-linked factors are analysed with regard to their influence on Ca(2+ )influx into neurons. Intensive cortex activity can render motor neurons susceptible to stimulation of calcium-permeable glutamate NMDA-receptors; increase in CSF concentrations of glutamate, glycine, and norepinephrine supposedly can intensify these receptors' activity. Elevated CSF levels of GABA and reduced levels of serotonin can promote Ca(2+ )influx through glutamate AMPA-receptors and voltage-gated channels of L-, N-, and P-type. Additionally, brain ischaemia can contribute to Ca(2+ )overload of motor neurons. Thus, ALS is characterized by the unique combination of factors potentially able to promote the overload of motor neurons with calcium.

Publication types

  • Review

MeSH terms

  • Amyotrophic Lateral Sclerosis / cerebrospinal fluid
  • Amyotrophic Lateral Sclerosis / pathology*
  • Amyotrophic Lateral Sclerosis / physiopathology*
  • Brain Chemistry / physiology
  • Calcium / metabolism*
  • Cell Death
  • Cerebral Cortex / physiopathology
  • Humans
  • Motor Neurons / metabolism*
  • Neurotransmitter Agents / cerebrospinal fluid
  • Receptors, Glutamate / physiology


  • Neurotransmitter Agents
  • Receptors, Glutamate
  • Calcium