@article{eprints3330,
         journal = {Brain Research Bulletin},
       publisher = {Elsevier},
          author = {Ulderico Freo and Mauro Dam and Gilberto Pizzolato and Pietro Pietrini and Timothy T. Soncrant and Leontino Battistin},
          volume = {621},
           pages = {175 -- 179},
          number = {1},
           title = {The monosialoganglioside \{GM1\} dose-dependently reduces regional cerebral metabolic rates for glucose in awake rats},
            year = {1993},
        keywords = {Monosialoganglioside GM1; Glucose metabolic rate; Cerebral metabolism; Excitatory amino acid; Hippocampus},
        abstract = {Using the quantitative autoradiographic 14C2-deoxyglucose technique, regional cerebral metabolis rats for glucose (rCMRglc) were measured in awake male Fischer-344 rats at 1,2,3,4 and 6 h after administration of {$\backslash$}\{GM1{$\backslash$}\} 30 mg/kg and at 3 h after {$\backslash$}\{GM1{$\backslash$}\} 150 or 300 mg/kg. {$\backslash$}\{GM1{$\backslash$}\} is a natural compound that is able to prevent neuron degeneration induced by exposure to excitatory amino acids in vitro and by ischemia or neurotoxins in vivo. {$\backslash$}\{GM1{$\backslash$}\} 30 mg/kg, a dose very effective in preventing excitatory amino acid-induced neurotoxicity, produced minimal rCMRglc change over a 6 h period. {$\backslash$}\{GM1{$\backslash$}\} 150 and 300 mg/kg reduced rCMRglc, in 14 (31\%) and in 29 (64\%) brain regions, respectively. Maximal metabolic effects occurred in hippocampal areas which possess, in specific subfields, the highest brain concentrations of different excitatory amino acid receptor subtypes. This finding suggests an effect by {$\backslash$}\{GM1{$\backslash$}\} on postreceptor mechanisms common to different excitatory amino acids.},
             url = {http://eprints.imtlucca.it/3330/}
}