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Local uptake of ^14^C‐labeled acetate and butyrate in rat brain in vivo during spreading cortical depression by Gerald A. Dienel; Kenian Liu; Nancy F. Cruz is a Neuroscience article available to read on EtoBox.

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## Abstract Spreading depression severely disrupts ion homeostasis, causes sensory neglect and motor impairment, and is associated with stroke and migraine. Glucose utilization (CMR~glc~) and lactate production rise during spreading depression, but the metabolic changes in different brain cell types are unknown. Uptake of ^14^C‐labeled compounds known to be preferentially metabolized by the glial tricarboxylic acid cycle was, therefore, examined during unilateral KCl‐induced spreading cortical depression in conscious, normoxic rats. [^14^C]Metabolites derived from [^14^C]butyrate in K^+^‐treated tissue rose 21% compared to that of untreated contralateral control cortex, whereas incorporation of H^14^CO~3~ into metabolites in K^+^‐treated tissue was reduced to 86% of control. Autoradiographic analysis showed that laminar labeling of cerebral cortex by both ^14^C‐labeled acetate and butyrate was elevated heterogeneously throughout cortex by an average of 23%; the increase was greatest (∼40%) in tissue adjacent to the K^+^ application site. Local uptake of acetate, butyrate, and deoxyglucose showed similar patterns, and monocarboxylic acid uptake was highest in the structures in which

Who reads Local uptake of ^14^C‐labeled acetate and butyrate in rat brain in vivo during spreading cortical depression?

Author

Gerald A. Dienel; Kenian Liu; Nancy F. Cruz

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

2001

Language

EN

Field

Neuroscience (Life Sciences)