​The non-invasive imaging of neuronal activity in the intact brain is of primordial importance to understand mechanisms underlying brain function both in humans and animal models. Most approaches, so far, have relied on the neurovascular coupling principle: neuronal activity results in a local increase in blood flow and metabolism (blood oxygenation level-dependent (BOLD)). However, the BOLD fMRI approach presents some limitations, as its link with neuronal activity remains indirect and fMRI responses may be significantly altered or even suppressed in situations interfering with the neurovascular coupling mechanisms (drugs and anesthesia).

Diffusion functional MRI (DfMRI) has been introduced as a novel tool to investigate the neuronal activation by looking at displacements of water molecules in tissues. Recently, we showed that DfMRI response was observed under nitroprusside, a neurovascular uncoupler, while BOLD fMRI response was suppressed (http://www.pnas.org/content/110/28/11636.full). This indicates that DfMRI signal is not of vascular origin; however, it remains unclear what the precise source of the DfMRI signal is. The objective of this project is to clarify the mechanisms of DfMRI response using a rodent animal model. We hypothesize that the DfMRI response is due to changes in cells' architecture (e.g., swelling of the neurons and/or astrocytes).