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Such a scheme serves as a template for the lactate shuttling present within the mammalian CNS. An nearly contemporaneous report extended this scheme to apply to the mammalian brain, however with notable variations and additions. It was to prove one of the most contentious papers in the sector of brain power metabolism and the debate raging round the topic persists. The paper described experiments carried out utilizing cultures of mouse cerebral neurones and astrocytes, and demonstrated a number of key options, which have been stoichiometrically strong (Pellerin and Magistretti, 1994). The background to the research was the realization that if metabolic signaling had been to occur between neurones and astrocytes in the mammalian CNS, there should exist a signaling mechanism whereby the neurones sign to astrocytes their need for delivery of metabolic substrate. The signaling mechanism will need to have the following traits: (1) it must be related to the frequency of activity of the neurones i.e., the discharge of the compound must be associated to the activity of the neurones, (2) it should be sensed by the astrocyte i.e., there have to be mechanism(s) whereby the astrocyte senses the molecule, and (3) there must exist a system or process whereby the focus of the molecule is decreased upon cessation of activity i.e., there should be an effective buffering system that reduces the concentration of the molecule after exercise.
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