This report demonstrates that during the torpor phase of hibernation, hamsters utilize ^<14>C and ^<13>C glucose in torpor specific brain metabolic pathways. Microdialysis of ^<14>C glucose into the striatum rapidly induced a steady state labelling of ECF lactate and labelling of tissue GABA, glutamate (GLU), glutamine (GLN) and alanine in ipsilateral and contralateral striata. The same tissue metabolites were labelled in cortex, hypothalamus and brainstem after microdialysis of ^<14>C lactate into the lateral ventricle. Serine, aspartate, glycine, taurine, tyrosine and methionine were not synthesised from glucose or lactate during torpor. ECF levels of amino and organic acids were low and unchanging during torpor and increased late during arousal to cenothermia. Labelled intracellular ^<14>C GABA and GLU were not communicated to the striatal ECF or ventricular space during torpor. ^<13>C NMR demonstrated rapid formation of lactate and functional TCA cycles in GABAergic and glutamatergic neurons, and enrichment of GLN and alanine after IV ^<13>C glucose. Large changes in tissue levels of amino acids occur prior to or during entrance into torpor but not during torpor. It is proposed that cerebral intracellular dehydration, the enlargement of ECF and the biochemistries associated with brain water homeostasis may have a role in regulating hibernation.
注記
The definitive version is available at www.blackwell-synergy.com
