Unlike systemic administration of p-chloroamphetamine, direct intracerebral injection does not produce degeneration of 5-HT axons

Exp Neurol. 1990 Sep;109(3):257-68. doi: 10.1016/s0014-4886(05)80015-9.

Abstract

Systemic administration of the amphetamine derivative p-chloroamphetamine (PCA) causes degeneration of 5-HT axon terminals in rat brain. The present study was designed to determine whether PCA induces neurotoxic effects by a direct action on 5-HT axon terminals. PCA was administered by microinjection directly into the cerebral cortex of rats. Continuous intracerebral infusions were made over extended time periods (10 min-48 h) to explore whether the induction of neurotoxicity requires a prolonged exposure of axon terminals to the drug. Two weeks after drug administration, brain sections that passed through the injection site were processed for 5-HT immunohistochemistry. The 5-HT innervation of cerebral cortex in PCA-injected animals was compared with that after intracortical injection of saline or of 5,7-dihydroxytryptamine. The results demonstrate that, in the concentrations used, direct application of PCA into the neocortex does not elicit axonal degeneration, even after a continuous infusion for 2 days. This finding suggests that PCA itself is not directly toxic to 5-HT axons.

Publication types

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

MeSH terms

  • 5,7-Dihydroxytryptamine / pharmacology
  • Animals
  • Axons / drug effects
  • Axons / metabolism*
  • Cerebral Cortex / physiology*
  • Immunohistochemistry
  • Injections
  • Male
  • Nerve Degeneration*
  • Rats
  • Rats, Inbred Strains
  • Serotonin / metabolism*
  • Sodium Chloride / pharmacology
  • p-Chloroamphetamine / administration & dosage*
  • p-Chloroamphetamine / pharmacology

Substances

  • 5,7-Dihydroxytryptamine
  • Serotonin
  • Sodium Chloride
  • p-Chloroamphetamine