Lesion of dopaminergic terminals in the amygdala produces enhanced locomotor response to D-amphetamine and opposite changes in dopaminergic activity in prefrontal cortex and nucleus accumbens

Brain Res. 1988 May 3;447(2):335-40. doi: 10.1016/0006-8993(88)91136-5.

Abstract

In a previous study using differential pulse voltammetry we demonstrated an interaction between dopaminergic activity in the amygdala and the nucleus accumbens. In the present study, by post-mortem biochemical measurements, we showed that bilateral 6-OHDA lesions of DA innervation of the amygdala leads to an increase in DA activity in the nucleus accumbens (DOPAC/DA ratio +24%) and a reduction (DOPAC/DA ratio -40%) in the prefrontal cortex. In addition, after these lesions in the amygdala, there was an increased behavioral sensitivity to D-amphetamine, demonstrated by enhanced locomotor activity. Increased understanding of the interregulations between dopaminergic activity in forebrain structures may help explain forebrain functions and/or dysfunctions.

MeSH terms

  • Amygdala / drug effects
  • Amygdala / physiology*
  • Animals
  • Cerebral Cortex / physiology*
  • Dextroamphetamine / pharmacology*
  • Dopamine / physiology*
  • Hydroxydopamines / pharmacology
  • Locomotion / drug effects*
  • Male
  • Nucleus Accumbens / physiology*
  • Oxidopamine
  • Rats
  • Rats, Inbred Strains
  • Septal Nuclei / physiology*

Substances

  • Hydroxydopamines
  • Oxidopamine
  • Dextroamphetamine
  • Dopamine