[18F]haloperidol binding in baboon brain in vivo

Khalil A. Yousef, Joanna S. Fowler, Nora D. Volkow, Stephen L. Dewey, Colleen Shea, David J. Schlyer, S. John Gatley, Jean Logan, Alfred P. Wolf

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


The binding of [18F]haloperidol to dopamine D2 and to sigma recognition sites in baboon brain was examined using positron emission tomography (PET). Studies were performed at baseline and after treatment with either haloperidol (to evaluate saturability), (+)-butaclamol (which has specificity for dopamine D2 receptors) or (-)-butaclamol (which has specificity for sigma sites). Binding was widespread. Treatment with (-)-butaclamol had no effect, whereas (+)-butaclamol selectively reduced the uptake in striatum. Haloperidol increased the clearance rate from all brain regions. These results indicate that the binding profile of [18F]haloperidol does not permit the selective examination of either dopamine D2 or sigma sites using PET.

Original languageEnglish
Pages (from-to)47-52
Number of pages6
JournalNuclear Medicine and Biology
Issue number1
StatePublished - Jan 1996
Externally publishedYes


  • Dopamine D2 receptors
  • PET
  • Sigma binding sites
  • [F]haloperidol


Dive into the research topics of '[18F]haloperidol binding in baboon brain in vivo'. Together they form a unique fingerprint.

Cite this