Anderson J S
Department of Neuroradiology, University of Utah, Salt Lake City, Utah, USA.
AJNR Am J Neuroradiol. 2008 Oct;29(9):1722-9. doi: 10.3174/ajnr.A1220. Epub 2008 Jul 17.
Low-frequency (<0.08 Hz) fluctuations in spontaneous blood oxygen level-dependent (BOLD) signal intensity show synchronization across anatomically interconnected and functionally specific brain regions, suggesting a neural origin of fluctuations. To determine the mechanism by which high-frequency neural activity results in low-frequency BOLD fluctuations, I obtained measurements of the effects of neurovascular coupling on the frequency content of BOLD fluctuations.
3T recordings of BOLD signal intensity in the primary visual cortex were obtained in response to visual stimuli presented at varying temporal frequencies to determine which stimulus frequencies were successfully transmitted to BOLD signal intensity. Additional BOLD time series recordings were performed in a resting state and during natural visual stimulation, and frequencies comprising BOLD fluctuations were measured. Magnetoencephalographic (MEG) time series recordings were obtained in a resting state to measure which components of MEG signal intensity best correlated in frequency distribution to observed BOLD fluctuations.
Visually driven oscillations in BOLD signal intensity were observed up to 0.2 Hz, representing a mismatch between low-pass filter properties of neurovascular coupling and observed frequencies of spontaneous BOLD fluctuations, which are <0.05 Hz in the primary visual cortex. Visual stimulation frequencies of >0.2 Hz resulted in frequency-dependent increases in mean BOLD response. Amplitude modulation of high-frequency neural activity was measured in MEG time series data, which demonstrated 1/frequency distribution with the greatest power comprising frequencies <0.05 Hz, consistent with the distribution of observed BOLD fluctuations.
Synchronized low-frequency BOLD fluctuations likely arise from a combination of vascular low-pass filtering and low-frequency amplitude modulation of neural activity.
自发血氧水平依赖(BOLD)信号强度的低频(<0.08Hz)波动显示出在解剖学上相互连接且功能特定的脑区之间的同步性,提示波动具有神经起源。为了确定高频神经活动导致低频BOLD波动的机制,我获取了神经血管耦合对BOLD波动频率成分影响的测量结果。
在初级视觉皮层中,针对以不同时间频率呈现的视觉刺激,获取3T的BOLD信号强度记录,以确定哪些刺激频率成功传递至BOLD信号强度。在静息状态和自然视觉刺激期间进行额外的BOLD时间序列记录,并测量构成BOLD波动的频率。在静息状态下获取脑磁图(MEG)时间序列记录,以测量MEG信号强度的哪些成分在频率分布上与观察到的BOLD波动最相关。
观察到高达0.2Hz 的由视觉驱动的BOLD信号强度振荡,这代表了神经血管耦合的低通滤波器特性与观察到的自发BOLD波动频率之间的不匹配,在初级视觉皮层中自发BOLD波动频率<0.05Hz。>0.2Hz的视觉刺激频率导致平均BOLD反应随频率增加。在MEG时间序列数据中测量了高频神经活动的幅度调制,其显示出1/频率分布,最大功率包含<0.05Hz的频率,与观察到的BOLD波动分布一致。
同步的低频BOLD波动可能源于血管低通滤波和神经活动的低频幅度调制的组合。