Neurotoxin induced nerve cell degeneration: possible involvement of calcium.
Neurotoxin induced nerve cell degeneration has been studied in sensory ganglia of newborn and in the area postrema of adult rats following the administration of the selective sensory neurotoxin, capsaicin and the amino acid excitotoxin, glutamic acid, respectively. Light microscopic histochemical, autoradiographic, electroncytochemical and X-ray microanalytical studies revealed that degeneration of certain small-sized, type B primary sensory neurons, induced by capsaicin, was associated with a marked accumulation of calcium predominantly in mitochondria of the damaged ganglion cells. Similarly, monosodium glutamate treatment resulted in the appearance of calcium-containing electron-dense granules in mitochondria of degenerating area postrema neurons. In addition, after a combined administration of 45Ca2+ and capsaicin or monosodium glutamate, significantly higher levels of radioactivity have been detected by liquid scintillation spectroscopy in the Gasserian ganglia and the area postrema, respectively. It is concluded that an enhancement in intracellular calcium level may be intimately involved in the process of neuronal cell death and may represent a common basic mechanism responsible for the development of cellular events leading ultimately to the degeneration of nerve cells.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002211:Capsaicin / Q000494:pharmacology*; D002470:Cell Survival; D005971:Glutamates / Q000494:pharmacology*; D006651:Histocytochemistry; D009410:Nerve Degeneration / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012970:Sodium Glutamate / Q000494:pharmacology*
D005971:Glutamates; D002211:Capsaicin; D002118:Calcium; D012970:Sodium Glutamate