Neuronal activation is accompanied by a local increase in cerebral blood flow (CBF) and in cerebral metabolic rate of oxygen (CMRO(2)), caused by neurovascular and neurometabolic coupling. Hypothermia is used as a neuroprotective approach in surgical patients and therapeutically after cardiac arrest or stroke. The effect of hypothermia on neurovascular coupling is of interest for evaluating brain function in these patients, but has not been determined so far. It is not clear whether functional hyperaemia actually operates at subnormal temperatures. In addition, decreasing brain temperature reduces spontaneous CMRO(2) following a known quantitative relationship (Q(10)). Q(10) determination may serve to validate a recently introduced CMRO(2) measurement approach relying on optical measurements of CBF and hemoglobin concentration. We applied this method to investigate hypothermia in a functional study of the somatosensory cortex. Anesthetized Wistar rats underwent surgical implantation of a closed cranial window. Using laser Doppler flowmetry and optical spectroscopy, relative changes in CBF and hemoglobin concentration were measured continuously. At the same time, an electroencephalogram (EEG) was recorded from the measurement site. By the application of ice packs, whole-body hypothermia was induced, followed by rewarming. Spontaneous EEG, CBF and CMRO(2) were measured, interleaved by blocks of electrical forepaw stimulation. The Q(10) obtained from spontaneous CMRO(2) changes of 4.4 (95% confidence interval 3.7-5.1) was close to published values, indicating the reliability of the CMRO(2) measurement. Lowering brain temperature decreased functional changes of CBF and CMRO(2) as well as amplitudes of somatosensory evoked potentials (SEP) to the same degree. In conclusion, neurovascular and neurometabolic coupling is preserved during hypothermia.