Journal of Neuroscience, Vol 8, 3920-3928, Copyright © 1988 by Society for Neuroscience
Effects of nicotine on local cerebral glucose utilization in the rat
ED London, RJ Connolly, M Szikszay, JK Wamsley and M Dam
Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224.
We used the autoradiographic 2-deoxy-D-[1-14C]glucose (14C-DG) method of
Sokoloff to identify brain areas with altered rates of local cerebral
glucose utilization (LCGU) in vivo in response to peripheral I- nicotine
administration (0.1, 0.3, 1.0, and 1.75 mg/kg, s.c.). Nicotine stimulated
LCGU primarily in areas reported to contain nicotine binding sites,
indicating that the sites are true receptors. Increases in LCGU of 100% or
more over control were obtained in the medial habenula, fasciculus
retroflexus, superior colliculus, and median eminence. Substantial
stimulation (50-100% increases) also was obtained in the cerebellar vermis,
interpeduncular nucleus, and anteroventral and interanteromedial thalamic
nuclei. Moderate increases (20-50%) were observed in the reticular nucleus
of the medulla, paramedian lobule, nucleus of the spinal tract of the
trigeminal nerve, presubiculum, subiculum, red nucleus, ventral tegmental
area, substantia nigra, nucleus ambiguus, nucleus tractus solitarius,
dorsal lateral geniculate nucleus, mammillothalamic tract, and fornix. The
greatest stimulation in most affected areas was obtained with 0.3 mg/kg
nicotine administered at 2 min, but not longer, before 14C-DG. Effects of
nicotine on LCGU were antagonized by mecamylamine. The findings indicate
that the interaction of nicotine with specific binding sites is coupled to
cerebral energy metabolism. The distribution of in vivo cerebral metabolic
effects of nicotine implicates various brain regions in the behavioral and
physiological effects of nicotine.
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