Lack of recovery in K+-dependent dopamine release and D2 receptor binding after cardiac arrest and reperfusion

Folia Neuropathol. 2003;41(3):139-44.

Abstract

The aim of the study was to assess the effects of global cerebral ischaemia (caused by temporary cardiac arrest and early (1, 24 h) and late (7 days) consequences of reperfusion) on the sensitivity of K+-dependent dopamine release from synaptosomes and D2 receptor binding sites. The rate of K+-dependent dopamine release decreased after 10 min cardiac arrest (70% of control). This effect was slightly enhanced after 1 h, 24 h and 7 days post-reperfusion; there was no possibility of recovery after 7 days post-reperfusion. Simultaneously, we observed increased dopamine D2 receptor affinity (decreased KD) and reduction of D2 receptor binding sites (Bmax) in the early post-reperfusion phase. No recovery was observed after extending the period to 7 days. Present observations are different from previously published data, which show almost full recovery in release of GABA and GABA(B) receptor binding. It seems that cardiac arrest-induced ischaemic insult can cause selective alterations in dopaminergic transmission. Lack of possibility to recover dopamine release and activity of dopamine D2 receptor after 7 days post-reperfusion can be associated with irreversible injury of dopaminergic neurones, which can be involved in several dysfunctions of the brain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dopamine / metabolism*
  • Heart Arrest / metabolism*
  • Male
  • Myocardial Reperfusion Injury / metabolism*
  • Potassium / pharmacology*
  • Protein Binding / drug effects
  • Protein Binding / physiology
  • Rats
  • Rats, Wistar
  • Receptors, Dopamine D2 / metabolism*
  • Synaptosomes / drug effects
  • Synaptosomes / metabolism

Substances

  • Receptors, Dopamine D2
  • Potassium
  • Dopamine