12 January 2009

Myles Jones to speak at Harvard Medical School

In January 2009, Dr Myles Jones will speak at the Martinos Centre for Biomedical imaging as part of their brain mapping seminar series. The Martinos Centre is part of both Harvard Medical School and the Massachusetts Institute of Technology. The seminar will outline research being conducted at the University of Sheffield Psychology Department that measures changes in cerebral blood flow and metabolism that occur when the amount of electrical activity in the brain increases. How this research may aid the interpretation of data from neuroimaging techniques such as functional magnetic resonance imaging (fMRI) will be discussed.

An abstract of the talk is included below:

Stimulus-Evoked Neurovascular and Metabolic Coupling Relationships in Rodent Somatosensory Cortex
Blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) relies on changes in cerebral blood flow, blood volume and blood oxygenation (collectively referred to as the hemodynamic response) that accompany increases in evoked neural activity produced by stimulus presentation or task. As such, data from such techniques can be difficult to correctly interpret in terms of the underlying cerebral activity. As in the MGH laboratory, at Sheffield, optical techniques (LDF, optical imaging spectroscopy) have been used to characterise the cortical hemodynamic response function in rodents following presentation of sensory stimuli. Combinations of optical, MRI and multi-depth electrophysiological techniques have allowed investigation of the quantitative relationships between evoked activity and hemodynamics that underpin fMRI. To attempt to clarify the role of the hemodynamic response in terms of oxygen delivery to brain, the changes in cortical tissue oxygenation during activation were characterised by making polarographic electrode measurements. While recording from superficial cortical locations (1- ~600 µm) ‘electrical’ whisker-pad stimuli typically evoked decreases in brain tissue oxygenation while at deeper cortical locations (~700-1400µm) increases in oxygenation were observed. Similar cortical ‘depth-profiles’ of tissue oxygenation changes could be observed following presentation of stimuli to individual vibrissa. Finally, while recordings were made at superficial depths (~300µm) the spatial extent of cortical activation was varied by either presenting stimuli to the individual whisker (C1) corresponding to the topographic placement of the electrode or to ‘neighbouring’ rows of mystacial vibrissae on the whisker pad (rows D and E). Stimuli presented to whisker C1 again produced decreases in tissue oxygenation while the evoked tissue oxygen response to ‘neighbouring-rows’ stimuli was characterised by increases in cortical tissue oxygen preceded by a smaller initial decrease. These data suggest that the relative degrees of cortical ‘hyper-’ and deoxygenation observed during cortical activation may depend on both the spatial extent of activation and cortical depth location of the recording electrode.

Martinos Center for Biomedical Imaging