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. 2002 Sep 20;950(1-2):119-26.
doi: 10.1016/s0006-8993(02)03011-1.

Effects of cue exposure on brain glucose utilization 8 days after repeated cocaine administration

Clifford M Knapp  1 , Bella Printseva, Nicole Cottam, Conan Kornetsky
Affiliations

Effects of cue exposure on brain glucose utilization 8 days after repeated cocaine administration

Clifford M Knapp et al. Brain Res. .

Abstract

Relapse to cocaine use may involve exposure to cocaine-associated environmental cues. The present experiment tested the hypothesis that basal local cerebral metabolic rate for glucose (LCMR(glu)), as measured by the 2-deoxy-D-[l-(14)C]glucose (2-DG) autoradiography, would change in the presence of cocaine conditioned cues at 8 days after the last of seven daily cocaine injections (30 mg/kg). This dose regimen results in sensitization to the locomotor effects of cocaine. Cocaine was administered to two groups of rats while saline was administered to a third. In the conditioned group, the rats were placed into the 2-DG experimental chamber immediately after cocaine injection. Rats in the non-conditioned group were placed into their home cage after cocaine administration. A control group received only saline. The 2-DG experiment was conducted in non-drugged animals 8 days after treatment completion. The interaction between treatment status and brain region was significant. Mean basal LCMR(glu) was significantly lower in 12 brain regions in the conditioned group as compared to the control group, but was significantly lower in only four areas in the non-conditioned group. Regions in which there were significant changes in the conditioned group included the basolateral amygdala, subiculum, medial thalamus, lateral habenula and the substantia nigra pars compacta. LCMR(glu) was significantly reduced in the ventrolateral orbital cortex and rostral nucleus accumbens in both experimental groups. These findings indicate that repeated cocaine administration can cause protracted decreases in basal LCMR(glu), decreases that are more widespread in the brain during exposure to cocaine-associated cues.

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