Altered metabolic activity in the cerebral cortex of rats exposed to ketamine

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Abstract
Uptake of the metabolic marker, [3H]2‐deoxy‐D‐glucose(2DG) was compared in rats given subanesthetic (50–100 mg/kg, i.p.) or anesthetic (200 mg/kg, i.v.) doses of ketamine with that in normal, unanesthetized rats. All doses of ketamine caused a relative increase of 2DG labeling in limbic regions, including the hippocampus, dentate gyrus, and cingulate, piriform, and entorhinal cortices. Striking 2DG‐dense zones were confined to the molecular layer in the hippocampus, dentate gyrus, and entorhinal cortex. Sub‐anesthetic doses of ketamine produced a relative reduction of 2DG uptake in layers 1‐1V of granular somalosensory cortex while sparing up take in layer Va; therefore, the peak of dense uptake shifted from layer IV to layer Va. In regions of the somatosensory cortex which display a dysgranular layer IV, vertical columns of relatively dense 2DG uptake extended through all cortical layers. Columns of 2I) G label also occurred outside of S1, in visual and auditory areas. In the primary visual cortex, this dose of ketamine decreased 2DG uptake relative to secondary visual cortex.Alteration of 2DG uptake in various cortical regions might be the consequence of a ketamine‐induced activation of specific neuronal pathways with special neurochemical features. During subanesthetic ketamine administration, peak 2DG uptake shifts from cortical layer IV, which receives specific thalamocortical input to layer Va which receives projections via intrinsic cortical circuits. The ketamine‐induced shift in the laminar focus of sensory cortical metabolism may reflect a functional disconnection from peripheral sensory input and/or enhanced internal (corticocortical) processing. These changes are more apparent during ketamine administration at doses too low to induce anesthesia and may, therefore, reflect the metabolic events that occur when ketamine and its analogues are taken as drugs of abuse.