Visual activation in alpha-chloralose-anaesthetized cats does not cause lactate accumulation in the visual cortex as detected by [1H]NMR difference spectroscopy.

The hypothesis that neuronal activation results in lactate accumulation due to mismatch between glucose and oxygen consumption was tested in the cat model of visual activation by monitoring cerebral metabolism with localized 1H nuclear magnetic resonance spectroscopy (MRS). Adult cats were anaesthetized with alpha-chloralose, paralysed and mechanically ventilated. Visual evoked potentials measured over the occipital cortex showed maximal amplitude at 2 Hz stimulation, but the latencies of the early cortical potentials, N1 and P1, were independent of stimulation frequency. High signal-to-noise ratio, short echo time volume-selected [1H]MRS was used to monitor cerebral lactate with a temporal resolution of 70 s. Difference proton spectroscopy unambiguously showed no lactate peak in the visual cortex during visual activation at stimulation frequencies ranging from 1 to 16 Hz. Absence of change in lactate concentration during visual stimulation was confirmed by averaging all the spectra acquired during activation and subtracting them from reference spectra collected in darkness, a procedure that had a calculated lactate detection limit of 0.17 mM. We also reduced the O2 in the inspired air to 13%, which decreased pO2 from 94.5 +/- 8.9 to 47.0 +/- 6.8 mmHg, during visual stimulation at 2 or 4 Hz. At this low PO2 level, visual stimulation did not cause lactate accumulation in the visual cortex, however. The present data show that neuronal activation to this degree in the cat brain is not associated with aerobic lactate production to an extent that can be detected with 1H MRS.