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NEUROLOGY 1998;51:1297-1302
© 1998 American Academy of Neurology

Muscarinic cholinergic receptors in human narcolepsy

A PET study

Y. Sudo, MD, T. Suhara, MD, PhD, Y. Honda, MD, PhD, T. Nakajima, MD, Y. Okubo, MD, PhD, K. Suzuki, PhD, Y. Nakashima, MD, PhD, K. Yoshikawa, MD, PhD, T. Okauchi, MSc, Y. Sasaki, MD, PhD and M. Matsushita, MD, PhD

From the Division of Advanced Technology for Medical Imaging (Drs. Sudo, Suhara, Okubo, Suzuki, and Yoshikawa, T. Okauchi, and Dr. Sasaki), National Institute of Radiological Sciences, Chiba; Department of Neuropsychiatry (Drs. Sudo, Nakajima, Nakashima, and Matsushita), Faculty of Medicine, University of Tokyo; Seiwa Hospital (Dr. Honda), Neuropsychiatric Research Institute; and Core Research for Evolutional Science and Technology (CREST) (Drs. Sudo and Suhara, and T. Okauchi), Japan Science and Technology Corporation, Tokyo, Japan.

Address correspondence and reprint requests to Dr. Yasuhiko Sudo, Division of Advanced Technology for Medical Imaging, National Institute of Radiological Sciences, 4-9-1, Anagawa, Inage-ku, Chiba-shi 263-8555, Japan; e-mail: sudo_y{at}nirs.go.jp

Objectives: To investigate the function of the muscarinic cholinergic receptor (mAchR) in narcolepsy and the effects of pharmacotherapy on mAchRs.

Background: Muscarinic neural transmission serves as the main executive system in REM sleep. Studies in canine narcolepsy reported an increase in mAchRs in the pons.

Methods: The mAchRs of 11 drug naïve/free patients with narcolepsy and 21 normal controls were investigated using PET with [11C] N-methyl-4-piperidylbenzilate ([11C]NMPB). Measurements were done in the pons, thalamus, striatum, and cerebral cortex. Seven of the 11 patients also underwent additional PET scans after the alleviation of symptoms by pharmacotherapy.

Results: There were no differences in [11C]NMPB binding between the control and drug naïve/free patients in all areas analyzed. At the time of on-medication PET scan, [11C]NMPB binding in the thalamus was decreased, but only to a small degree compared with that by anticholinergic drugs.

Conclusion: The present results do not support the notion that the mAchR is the main site of action of pharmacotherapy in the marked clinical improvement of human cataplexy.

Supported by the PET project of the National Institute of Radiological Sciences of Japan and a Grant-in-Aid from the Japanese Ministry of Education [No. (2)08671075]. Y.S., T.S., and T.O. are supported by CREST.

Received February 17, 1998. Accepted in final form July 11, 1998.






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