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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? 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
Overview • 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
Conclusion • 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