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How well do we understand the neural origins of the fMRI BOLD signal?. Owen J Arthurs and Simon Boniface Trends in Neuroscience, 2002 Gillian Elizabeth Munro, Nov 19, 2002. The Current Paper.

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How well do we understand the neural origins of the fMRI BOLD signal?

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How well do we understand the neural origins of the fMRI BOLD signal?

Owen J Arthurs and Simon Boniface

Trends in Neuroscience, 2002

Gillian Elizabeth Munro, Nov 19, 2002

The Current Paper

  • Examines our current understanding of the neural basis of the fMRI BOLD signal, and the ways that this knowledge can be improved


  • What is BOLD imaging?

  • The haemodynamic response

  • Evoked potentials and local field potentials

  • Synaptic activity and action potentials

  • Excitatory and inhibitory activity

What is the fMRI BOLD signal?

  • Blood oxygenation level-dependant imaging (BOLD) is most common method of fMRI

  • Relies on the difference in magnetization between oxy- and deoxyhaemoglobin

  • It is assumed to correlate with neural activity

Haemodynamic Coupling

  • Link between blood oxygenation levels and neural activity is known as “neurovascular coupling”

  • Nature of this mechanism is unknown

The haemodynamic response and fMRI BOLD signals

Neuronal activity Nurovascular coupling

The haemodynamic response Detection

by the scanner

Evoked Potentials and Local Field Potentials

  • The BOLD response directly reflects an increase in neural activity, correlating with local field potentials (LFPs) and evoked potentials

  • Evoked potentials and LFPs reflect population synaptic activity, NOT neuronal firing rates

Evoked Potentials and Local Field Potentials Cont’d

  • There is a linear correlation between neuronal activity and the haemodynamic response

Synaptic activity

  • Action potentials and synaptic activity correlate with BOLD

  • There is evidence that activity of cortical cells does not substantially contribute to the brain’s metabolic activity

  • The main determinant of these changes is the re-establishment of ionic concentrations after synaptic activity

Relevance of this relationship

  • EPSPs and IPSPs influence synaptic firing rate

  • Thus, one would expect that spiking activity adapts quickly, while LFP activity may be maintained during stimulus presentation

  • This relationship is difficult to standardize and/or quantify, as it may vary across time and cortical areas

Relevance cont’d

  • Would expect that there is a linear relationship between action potential firing rate and synaptic metabolic activity

  • Would also expect a linear correlation between a linear correlation between BOLD and spiking activity, as:

  • Spiking activity is correlated with firing rates, and firing rates are correlated with the BOLD signal

BOLD and population activity

  • Unclear whether it can differentiate between small changes in large populations vs large changes in small populations

  • Also unclear whether takes into account changes in background activity (e.g. attention, cognitive states)

BOLD and attention

  • Not only are BOLD signals non-absolute, but there is also a variable relationship between action potentials and synaptic energy demand

  • Changes in attentional states could mask underlying neuronal changes

  • Thus, the the ability of BOLD to detect stimulus-correlated activity is unpredictable

BOLD and other neuronal events

  • BOLD has the potential to include other neuronal events:

    - Bursts

    - Oscillations

    - Changes in neuronal synchrony

Problems with global scaling techniques

  • In eliminating the effect of steady population firing, could lose information regarding changes in cognitive states such as attention and sensory arousal

BOLD and Inhibitory Activity

  • Inhibitory synaptic activity may modulate BOLD response by changing the metabolic demand, or by inducing net spiking activity

  • The energy needed to produce an action potential, or to recycle inhibitory neurotransmitters, may cancel out the reduction in activity of inhibited post-synaptic cells

Inhibitory Activity Cont’d

  • BUT it is unlikely that an area of cortex could sustain a high volume of inhibitory activity, therefore causing a high metabolic and low firing rate

  • ~ 20% of cells in the cerebral cortex are non-pyramidal inhibitory cells

  • There could be a lower metabolic demand during inhibition than during excitation

Evidence from cerebellar cells

  • The principle cells in the cerebellum are inhibitory

  • In rats, no correlation has been found between blood flow and cellular activity in this region

  • This could suggest that excitatory activity alone provides basis for BOLD

Does inhibition produce a change in the BOLD signal?

  • Inhibitory activity may modulate the BOLD signal in a variable way:

    - increasing it when the prevailing level of excitement is low

    - decreasing it when the prevailing level of excitement is high

  • The use of neural drugs such as GABA-mediated inhibitory blockers could shed light on this issue


  • BOLD signals are related to a number of factors

  • Evidence supports a correlation between BOLD and population synaptic activity

  • May also be correlated with cellular action potentials

  • In need of further investigation, especially regarding the relationship between electrical activity and the BOLD signal

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