Takashi Uehara1, Tomiki Sumiyoshi, Hiroko Itoh, Masayoshi Kurachi. 1. Department of Neuropsychiatry, University of Toyama Graduate School of Medicine and Pharmaceutical Science, 2630 Sugitani, Toyama 930-0194, Japan. uehara@med.u-toyama.ac.jp
Abstract
RATIONALE: Lactate, like glucose, has recently been found to be an energy substrate for neural activity. It is indicated that lactate is produced by astrocytes under the regulation of glutamatergic tone. OBJECTIVES: Using in vivo microdialysis technique, we measured extracellular lactate concentrations in the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) of rats. To investigate the role of the glutamate transporter in the modulation of footshock stress-induced energy demands in both brain regions, we attempted to determine whether the footshock stress-induced changes of extracellular lactate concentrations are attenuated by local perfusion of the glutamate uptake inhibitor dihydrokainate (DHK). RESULTS: Perfusion of 1.0 mM DHK produced an increase in basal extracellular lactate levels in the mPFC and BLA, whereas 0.1 mM DHK did not affect lactate concentrations in either region. DHK also attenuated stress-induced increment of extracellular lactate concentrations in the mPFC, and completely prevented it in the BLA. CONCLUSIONS: These results suggest that glutamate transporters regulate lactate availability in astrocytes and indicate that the rapid energy demand induced by glutamate contributes to local lactate production.
RATIONALE: Lactate, like glucose, has recently been found to be an energy substrate for neural activity. It is indicated that lactate is produced by astrocytes under the regulation of glutamatergic tone. OBJECTIVES: Using in vivo microdialysis technique, we measured extracellular lactate concentrations in the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) of rats. To investigate the role of the glutamate transporter in the modulation of footshock stress-induced energy demands in both brain regions, we attempted to determine whether the footshock stress-induced changes of extracellular lactate concentrations are attenuated by local perfusion of the glutamate uptake inhibitor dihydrokainate (DHK). RESULTS: Perfusion of 1.0 mM DHK produced an increase in basal extracellular lactate levels in the mPFC and BLA, whereas 0.1 mM DHK did not affect lactate concentrations in either region. DHK also attenuated stress-induced increment of extracellular lactate concentrations in the mPFC, and completely prevented it in the BLA. CONCLUSIONS: These results suggest that glutamate transporters regulate lactate availability in astrocytes and indicate that the rapid energy demand induced by glutamate contributes to local lactate production.
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