An fMRI study of neuronal interactions in face-selective areas of the brain.

Functionally activated sites usually have multiple specificities where coactivation is induced by inputs with different informational content. Using typical voxel-based functional mapping (univariate analysis), it is possible to show the presence of coactivation; however, it is not possible to distinguish whether coactivation occurs by independent or interactive processing units unless measurements are made at an extremely high spatial resolution. To address this problem, we have utilized the phenomenon of refractory suppression observable when two stimuli were given with a temporal separation of approximately 100 ms. This phenomenon is known to be noticeable in primary sensory areas. In this study, refractory suppression was investigated to determine its possible applications in higher functional sites. Two visual stimuli were presented in different hemifields, using a paradigm in which the first of the paired stimuli (face pictures) was placed in the left visual hemifield and the second stimulus was placed in the right hemifield. In this manner, the primary visual areas (V1) of the left and right hemispheres were independently activated. Along with independent activation in both V1, refractory suppression was indeed observed in higher functional areas, including the occipital and fusiform face areas in both hemispheres.

Functional characteristics of TRPC4 channels expressed in HEK 293 cells.

The classical type of transient receptor potential (TRPC) channel is a molecular candidate for Ca(2+)-permeable cation channels in mammalian cells. Because TRPC4 and TRPC5 belong to the same subfamily of TRPC, they have been assumed to have the same physiological properties. However, we found that TRPC4 had its own functional characteristics different from those of TRPC5. TRPC4 channels had no constitutive activity and were activated by muscarinic stimulation only when a muscarinic receptor was co-expressed with TRPC4 in human embryonic kidney (HEK) cells. Endogenous muscarinic receptor appeared not to interact with TRPC4. TPRC4 activation by GTPgammaS was not desensitized. TPRC4 activation by GTPgammaS was not inhibited by either Rho kinase inhibitor or MLCK inhibitor. TRPC4 was sensitive to external pH with pK (a) of 7.3. Finally, TPRC4 activation by GTPgammaS was inhibited by the calmodulin inhibitor W-7. We conclude that TRPC4 and TRPC5 have different properties and their own physiological roles.