J Neuropsychiatry Clin Neurosci 11:209-221, May 1999
© 1999 American Psychiatric Press, Inc.
The EEG and Cocaine Sensitization
A Hypothesis
Kenneth R. Alper, M.D.
Received November 9, 1998; revised January 25, 1999; accepted February 8, 1999. From the Brain Research Laboratories and Comprehensive Epilepsy Center, Departments of Psychiatry and Neurology, New York University School of Medicine, New York, New York. Address correspondence to Dr. Alper, Brain Research Laboratories, New York University School of Medicine, Old Bellevue Administration Bldg., 462 First Avenue, New York, NY 10016.
The author presents the hypothesis that reduced delta EEG power observed in cocaine withdrawal is related to changes in dopamine (DA) transmission related to cocaine sensitization. Evidence for this hypothesis includes the topographic anatomical correspondence between the putative site of delta generation and the cortical terminal field of the mesotelencephalic DA system, as well as the laminar distribution and ultrastructural features of DA terminals in frontal cortex that appear to be adapted to the modulation of the delta rhythm, a global forebrain EEG mode. The effect of DA on membrane conductances of individual pyramidal neurons also suggests that DA exerts a significant influence on delta power by modulating the transition between global and local EEG modes. Access to a neural correlate of sensitization via noninvasive EEG methodology could be useful in investigating the relationship of stimulant sensitization to the clinical syndrome of cocaine dependence.
Key Words: Electroencephalography • Cocaine • Dopamine • Sensitization
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