A PET Study on the Acute Effect of Ethanol on Striatal D2 Dopamine Receptors with [[sup 11] C]Raclopride in Healthy Males.

The effect of acute oral ethanol intake (1·0 g/kg) on cerebral D2-receptors ([[sup 11] C]raclopride binding) was studied in seven healthy volunteers, using water and alcohol in two separate 59-min PET sessions. In the alcohol experiments, the blood ethanol concentration at the beginning of the imaging was 26·4±3·8 mmol/l and remained stable during the PET session. Ethanol was not found to influence binding of [[sup 11] C]raclopride to the dopamine D2 receptors in the human striatum, as indicated by the unchanged ratio B [sub max] /K [sub d] of the whole (left and right) striatum. The T [sub max] values of the control and ethanol experiments did not differ in the whole striatum, but the right to left difference of striatal T [sub max] was turned from negative to positive by ethanol (P =0·02). However, the difference between hemispheres in B [sub max] /K [sub d] was not significantly altered by ethanol intake. There was considerable interindividual variation in the response of all the above parameters to acute ethanol exposure. According to the present results, the acute effects of peroral ethanol exposure on striatal D2 receptor binding potential are of relatively small magnitude in man. However, the changes in T [sub max] suggest that ethanol may influence the right–left difference of [[sup 11] C]raclopride binding. © 1997 by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]