Uses, misuses, new uses and fundamental limitations of MRI in cognitive science
Professor Robert Turner, Max Planck Institute for Human Cognitive and Brain Sciences, Germany
When BOLD contrast was discovered in the early 1990s, it provoked an explosion of interest in exploring human cognition using brain mapping techniques based on MRI. Standards for data acquisition and analysis were rapidly put in place, in order to assist comparison of results across laboratories. Recently, MRI data acquisition capabilities have improved dramatically, inviting a rethink of strategies for relating functional brain activity at the systems level with its neuronal substrates and functional connections. This presentation will review the following questions:
a) What can structural and functional BOLD MRI reveal about human cognition that other techniques cannot provide?
b) In which areas of cognitive science has fMRI made major contributions?
c) What are the implicit assumptions underlying now-popular analysis techniques, and what are the flaws in these assumptions?
d) Can MRI-based myeloarchitectural parcellation of the cortex and high resolution fMRI methodology make these assumptions unnecessary?
e) Are there other ways of analyzing MRI/fMRI data that provide deeper insight?
f) Will cortical layer-specific fMRI enable questions of causality to be addressed, and what are the best candidate techniques for such acquisitions?
g) What are the likely fundamental limitations of all MRI and fMRI methods?
Neurovascular coupling: when its reliability as a marker of neuronal activity gets challenged
Professor Edith Hamel, Montreal Neurological Institute, McGill University, Canada
Changes in neuronal activity are spatially and temporally coupled to concurrent changes in cerebral blood flow (CBF), a process known as neurovascular coupling (NVC) that forms the basis of several brain imaging techniques. Yet, it is unclear how reliable this coupling remains during altered brain states and, particularly, under pathological conditions. Using the whisker-to-barrel pathway, a well-established model of NVC, we tested whether the coupling between neuronal activity and CBF would be affected by changes in brain states induced by varying the levels of acetylcholine (ACh), a potent modulator of sensory processing. Under acute increases in ACh tone, whisker-evoked hemodynamic responses and neuronal signals (LFPs and band-limited power) were potentiated despite no change in the extent and identity of the neuronal network recruited within the activated barrel. Inversely, chronic ACh deprivation compacted the activated barrel and reduced both sensory-evoked hemodynamic and neuronal responses. Our findings indicate that hemodynamic signals dependably reflect changes in the activity of the neural circuit underlying sensory processing under states of enhanced ACh neurotransmission and in conditions of a cholinergic deprived network as seen in Alzheimer’s disease.
Vasomotion: a link from ultra-slow neuronal activity to blood oxygenation
Professor David Kleinfeld, University of California, San Diego, USA
The blood-oxygenation-level-dependent (BOLD) fMRI signal is a central technology of modern cognitive neuroscience. An intriguing issue is that ultra-slow variations (~ 0.1 Hz) in the oxygenation of brain tissue appear to be mirrored across conjugate brain areas in the two hemispheres. This is referred to as ‘resting-state’ BOLD fMRI and this finding has been inverted in many studies of human cognition, so that ultra-slow co-fluctuations are interpreted as ‘function connections’. Yet the mechanism to support this interpretation remains to be discovered. Here we address this relation in awake mice through measurements of neuronal activity, tissue oxygenation, and conventional and ultra-large field two-photon imaging of vascular dynamics. We provide evidence that arteriole vasomotion can link ongoing, coordinated neuronal activity with ultra-slow oscillations in blood oxygenation. This result may justify inferring neuronal connections from synchronous ultra-slow vasodynamics between different brain areas.
Model-based approaches that connect BOLD imaging and dopaminergic transmission in humans
Professor Read Montague, Virginia Tech Carilion Research Institute, USA and University College London, UK
Using a simple sequential decision task we provide new data showing a cross cohort relationship between BOLD responses during the decision task and sub-second electrochemical estimates of dopamine and serotonin from the dorsal striatum. Not surprisingly the relationship among these three separate measures is not simple even allowing for the possibility that some features of the signaling are unique to the state of the subjects’ brains (i.e. Parkinson’s Disease or Essential Tremors). Dopamine and serotonin appear to correlate with error signals for experienced rewards and one form of counterfactual signals (what might have been gained or loss had the choice been different). Moreover, fluctuations in these two transmitters prospectively encode a subject’s strategy on their next choice (stay or shift) with dopamine carrying this information following a positive prediction error and serotonin carrying it following a negative prediction error. We speculate about the connection between the measured BOLD response and the measured neuromodulator response; however the results do suggest more complexity than is latent is models built solely around the BOLD response.