Effects of amphetamine and evoked dopamine release on [11C]raclopride binding in anesthetized cats.

The effects of halothane and ketamine anesthesia on [11C]raclopride binding were assessed in the cat striatum at basal conditions and after drug- or depolarization-induced dopamine (DA) release using Positron Emission Tomography. At baseline, Scatchard analyses revealed that the higher [11C]raclopride binding found under halothane anesthesia was mainly attributable to a higher radioligand apparent affinity. Decreased [11C]raclopride binding was demonstrated following amphetamine under ketamine but not under halothane anesthesia. Under ketamine anesthesia transient DA overflows induced by direct stimulations of DA neurons through an intracerebral electrode induced transient changes in [11C]raclopride binding with a remarkable spatiotemporal accuracy. No effect was observed under halothane anesthesia. The failure to detect competition between DA and [11C]raclopride for binding on D(2)-receptors under halothane anesthesia might reflect, as already reported for other brain receptor systems, a halothane-promoted conversion of D(2)-receptors to a state of lower affinity for DA. It is suggested that the affinity state of receptors is a factor to be considered in in vivo ligand-activation studies.