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Regulation of oxygen transport during brain activation: stimulus-induced hemodynamic responses in human and animal cortices

Akitoshi Seiyama1,2 email, Junji Seki3 email, Hiroki C Tanabe1 email, Yasuhiro Ooi4 email, Yasuhiko Satomura2,3 email, Hisao Fujisaki5 email and Toshio Yanagida1,2 email

1Kansai Advanced Research Center, Communications Research Laboratory, 588-2 Iwaoka, Nishi-ku, Kobe, Hyogo 651-2492, Japan

2Division of Physiology and Biosignaling, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan

3Department of Biomedical Engineering, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan

4Division of Pathogenesis and Control of Oral Disease, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan

5Nikon Corp. Business Development Center, 1-6-3 Nishi-Ooi, Shinagawa, Tokyo 140-8601, Japan

author email corresponding author email

Dynamic Medicine 2003, 2:6doi:10.1186/1476-5918-2-6

Published: 20 December 2003

Abstract

Background

The correlation between regional changes in neuronal activity and changes in hemodynamics is a major issue for noninvasive neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and near-infrared optical imaging (NIOI). A tight coupling of these changes has been assumed to elucidate brain function from data obtained with those techniques. In the present study, we investigated the relationship between neuronal activity and hemodynamic responses in the occipital cortex of humans during visual stimulation and in the somatosensory cortex of rats during peripheral nerve stimulation.

Methods

The temporal frequency dependence of macroscopic hemodynamic responses on visual stimuli was investigated in the occipital cortex of humans by simultaneous measurements made using fMRI and NIOI. The stimulus-intensity dependence of both microscopic hemodynamic changes and changes in neuronal activity in response to peripheral nerve stimulation was investigated in animal models by analyzing membrane potential (fluorescence), hemodynamic parameters (visible spectra and laser-Doppler flowmetry), and vessel diameter (image analyzer).

Results

Above a certain level of stimulus-intensity, increases in regional cerebral blood flow (rCBF) were accompanied by a decrease in regional cerebral blood volume (rCBV), i.e., dissociation of rCBF and rCBV responses occurred in both the human and animal experiments. Furthermore, the animal experiments revealed that the distribution of increased rCBF and O2 spread well beyond the area of neuronal activation, and that the increases showed saturation in the activated area.

Conclusions

These results suggest that above a certain level of neuronal activity, a regulatory mechanism between regional cerebral blood flow (rCBF) and rCBV acts to prevent excess O2 inflow into the focally activated area.


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