Local uptake of 14C-labeled acetate and butyrate in rat brain in vivo during spreading cortical depression

✍ Scribed by Gerald A. Dienel; Kenian Liu; Nancy F. Cruz

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 154 KB
• Volume: 66
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.10063

✦ Synopsis

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 apparent loss of labeled metabolites of [6‐^14^C]glucose was greatest. Enhancement of net uptake of acetate and butyrate in cerebral cortex during spreading depression is tentatively ascribed to increased astrocyte metabolism. © 2001 Wiley‐Liss, Inc.