Cocaine, in contrast to D-amphetamine, does not cause axonal terminal degeneration in neostriatum and agranular frontal cortex of Long-Evans rats

Life Sci. 1988;43(17):1403-9. doi: 10.1016/0024-3205(88)90307-4.

Abstract

Continuous three day administration via implanted minipumps of cocaine hydrochloride (50-450 mg/kg/day, sc and 100-250 mg/kg/day, iv) did not produce axonal degeneration in frontal agranular cortex or neostriatum that was detectable by Fink-Heimer silver staining or tyrosine hydroxylase immunolabeling. This is in contrast to the extensive axonal degeneration detectable in these regions following d-amphetamine sulfate (10-60 mg/kg/day) administered following an identical protocol. Doses of cocaine and amphetamine were equated using three measures: 1) weight loss, 2) lethality and 3) behavioral activation. Thus, cocaine resembles other catecholamine reuptake blockers and does not cause the neurodegenerative changes characteristic of other abused drugs that interact with the brain's dopamine systems.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / drug effects*
  • Axons / pathology
  • Behavior, Animal / drug effects
  • Cerebral Cortex / drug effects*
  • Cerebral Cortex / pathology
  • Cocaine / administration & dosage
  • Cocaine / toxicity*
  • Corpus Striatum / drug effects*
  • Corpus Striatum / pathology
  • Dextroamphetamine / administration & dosage
  • Dextroamphetamine / toxicity*
  • Dopamine / metabolism
  • Infusion Pumps
  • Male
  • Nerve Degeneration*
  • Rats
  • Weight Loss

Substances

  • Cocaine
  • Dextroamphetamine
  • Dopamine