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The rationale for this isn't identified however clearly shows that astrocytes do not oxidatively metabolize all of the glucose they take up. The putative function for this lactate is open to debate. It could also be released from the astrocyte as a type of energy substrate that is immediately available to axons on the onset of elevated exercise. This is supported by data from in vivo recordings of cat cortex wherein lactate sensors inserted into the cortex of a live cat quickly falls at the onset of experimentally induced activity. The non permanent dip is adopted by a rise in lactate in response to the steady stimulus (Hu and Wilson, 1997). The preliminary dip is assumed to be because of the onset of activity requiring an instantaneous enhance in delivery of substrate to the neurones. The lactate in the interstitial area meets this criterion. The latter increase in lactate is presumably because of the mechanism whereby neurones signal to astrocytes of their elevated power necessities, and the astrocytes reply by releasing lactate.