Spectroscopic analysis of changes in remitted illumination: the response to increased neural activity in brain.

Imaging of neural activation has been used to produce maps of functional architecture and metabolic activity. There is some uncertainty associated with the sources underlying the intrinsic signals. It has been reported that following increased neural activity there was little increased oxygen consumption ( approximately 5%), although glucose consumption increased by approximately 50%. The research we describe uses a modification of the Beer-Lambert Law called path-length scaling analysis (PLSA) to analyze the spectra of the hemodynamic and metabolic responses to vibrissal stimulation in rat somatosensory cortex. The results of the PLSA algorithm were compared with those obtained using a linear spectrographic analysis method (we refer to this as LMCA). There are differences in the results of the analysis depending on which of the two algorithms (PLSA or LMCA) is used. Using the LMCA algorithm, we obtain results showing an increase in the volume of Hbr at approximately 2 s, following onset of stimulation but no complementary decrease in oxygenated haemoglobin (HbO(2)). These results are similar to a previous report. In contrast, after using the PLSA algorithm, the time series of the chromophore changes shows no evidence for an increase in the volume of deoxygenated haemoglobin (Hbr). However, after further analysis of the time series from the PLSA using general linear models (GLM) to remove contributions from low frequency baseline oscillations, both the HbO(2) and Hbr times series of the response to stimulation were found to be biphasic with an early decrease in saturation peaking approximately 1 s after onset of stimulation followed by a larger increase in saturation peaking at approximately 3 s. Finally, following the PLSA-then-GLM analysis procedure, we do not find convincing evidence for an increase in cytochrome oxidation following stimulation, though we demonstrate the PLSA algorithm to be capable of disassociating changes in cytochrome oxidation state from changes in hemoglobin oxygenation.