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Volume 17, Number 8, Issue of April 15, 1997 pp. 2796-2806
Copyright ©1997 Society for Neuroscience

Effects of m-Chlorophenylpiperazine on Regional Brain Glucose Utilization: A Positron Emission Tomographic Comparison of Alcoholic and Control Subjects

Received Oct. 2, 1996; revised Jan. 17, 1997; accepted Jan. 27, 1997.

Daniel Hommer¹, Paul Andreasen¹, Daniel Rio¹, Wendol Williams¹, Urs Ruttimann¹, Reza Momenan¹, Alan Zametkin², Robert Rawlings¹, and Markku Linnoila¹

¹  Laboratory of Clinical Studies, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, and ²  Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-1256

m-Chlorophenylpiperazine (mCPP) is a mixed serotonin agonist/antagonist used extensively in psychiatric research. Alcoholics show blunted neuroendocrine responses to mCPP, and in some settings mCPP can induce craving for alcohol, particularly among early onset alcoholics. We used 2-[¹⁸F]-2-deoxy-D-glucose positron emission tomography to examine the effects of intravenously administered mCPP (0.08 mg/kg) on brain glucose utilization in a group of 18 male alcoholics and 12 healthy male control subjects. Differences between two sequential scans (the first followed placebo and the second followed mCPP) were evaluated statistically with a Gaussian random field-based method. Among healthy volunteers mCPP significantly increased brain glucose metabolism in the right medial and posterior orbital gyrus, the cerebellar hemispheres bilaterally, the left nucleus accumbens, the head of the caudate nucleus bilaterally, the anterior and medial-dorsal nuclei of the thalamus bilaterally, the middle frontal gyrus, the left insular cortex, the left middle temporal gyrus, and the posterior cingulate gyrus. Among alcoholic subjects mCPP significantly increased brain glucose metabolism in larger areas of the cerebellum and posterior cingulate than it did in healthy volunteers, but compared with the healthy volunteers, alcoholics showed a smaller area of mCPP-induced activation in the thalamus, almost no activation in the orbital cortices, and no activation at all in the head of the caudate nucleus or the middle frontal gyrus. These results suggest that a serotoninergic challenge activates basal ganglia circuits involving orbital and prefrontal cortices among healthy volunteers but that the response of these circuits is blunted among alcoholics.

Key words: alcoholism; serotonin; PET; m-chlorophenylpiperazine; striatum; thalamus; orbital cortex; frontal cortex

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