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Proc Natl Acad Sci U S A. 2012 Nov 6;109(45):18565-70. doi: 10.1073/pnas.1119125109. Epub 2012 Oct 18.

Negative blood oxygenation level dependent homunculus and somatotopic information in primary motor cortex and supplementary motor area.

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1
Department of Medical Neurobiology, Institute for Medical Research Israel-Canada, Faculty of Medicine, Hebrew University, Jerusalem 91220, Israel.

Abstract

A crucial attribute in movement encoding is an adequate balance between suppression of unwanted muscles and activation of required ones. We studied movement encoding across the primary motor cortex (M1) and supplementary motor area (SMA) by inspecting the positive and negative blood oxygenation level-dependent (BOLD) signals in these regions. Using periodic and event-related experiments incorporating the bilateral/axial movements of 20 body parts, we report detailed mototopic imaging maps in M1 and SMA. These maps were obtained using phase-locked analysis. In addition to the positive BOLD, significant negative BOLD was detected in M1 but not in the SMA. The negative BOLD spatial pattern was neither located at the ipsilateral somatotopic location nor randomly distributed. Rather, it was organized somatotopically across the entire homunculus and inversely to the positive BOLD, creating a negative BOLD homunculus. The neuronal source of negative BOLD is unclear. M1 provides a unique system to test whether the origin of negative BOLD is neuronal, because different arteries supply blood to different regions in the homunculus, ruling out blood-stealing explanations. Finally, multivoxel pattern analysis showed that positive BOLD in M1 and SMA and negative BOLD in M1 contain somatotopic information, enabling prediction of the moving body part from inside and outside its somatotopic location. We suggest that the neuronal processes underlying negative BOLD participate in somatotopic encoding in M1 but not in the SMA. This dissociation may emerge because of differences in the activity of these motor areas associated with movement suppression.

PMID:
23086164
PMCID:
PMC3494917
DOI:
10.1073/pnas.1119125109
[Indexed for MEDLINE]
Free PMC Article
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