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Contributions of glial cells to neuroenergetics have been the focus of extensive debate. Here we provide the first positron emission tomography (PET) evidence that activation of the astrocytic glutamate transport via GLT-1 triggers widespread but graded glucose uptake in the rodent brain. Our results highlight the need for a reevaluation of the interpretation of [18F]FDG PET data, whereby astrocytes would be recognized to contribute significantly to the [18F]FDG signal.

Connectome genetics seeks to uncover how genetic factors shape brain functional connectivity; however, the causal impact of a single gene's activity on whole-brain networks remains unknown. We tested whether the sole targeted deletion of the mu opioid receptor gene (Oprm1) alters the brain connectome in living mice. Hypothesis-free analysis of combined resting-state fMRI diffusion tractography showed pronounced modifications of functional connectivity with only minor changes in structural pathways. Fine-grained resting-state fMRI mapping, graph theory, and intergroup comparison revealed Oprm1-specific hubs and captured a unique Oprm1 gene-to-network signature. Strongest perturbations occurred in connectional patterns of pain/aversion-related nodes, including the mu receptor-enriched habenula node. Our data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/aversion circuitry, with major influence on negative affect centers. mouse brain connectivity | resting-state functional MRI | diffusion tensor imaging | mu opioid receptor | reward/aversion network N euronal connectivity is at the foundation of brain function (1) and the concept that brain connectivity patterns are dynamically shaped by experience, pathology, and genetics has gained increasing importance. In humans, MRI has opened the era of connectome/imaging genetics to elucidate how genetic factors affect brain organization and connectivity in healthy individuals and disease, and to correlate genotype to phenotype (2). However, the causal impact of a single gene on overall functional connectivity (FC) remains largely unknown, and animal research is best suited to this goal. Here we tested whether combined functional/structural MRI in live animals (3-8) coupled to open-ended postprocessing analysis would reveal connectivity alterations upon targeted inactivation of a single gene. The mu opioid receptor (MOR) mediates the remarkably potent analgesic and addictive properties of opiates, like morphine (9), and belongs to the endogenous opioid system that controls sensory, emotional, and cognitive processes. This receptor is broadly distributed throughout the nervous system (10). It is a key component to facilitate reward (11) and relieves the negative experience of pain (12)(13)(14). In this report we show that targeted deletion of the MOR gene (Oprm1) significantly alters the brain connectome in living mice and predominantly reshapes the so-called reward/aversion network involved in pain, depression, and suicide (15). Results and DiscussionFine-Grained Mapping of the Mouse Brain Functional Connectome. In a first step, we established fine-grained mapping of the mouse brain functional connectome (MBFC) in control and Oprm1 −/− living mice. Using data-driven spatial independent component analysis (100-ICASSO) (4) of combined blood oxygenation level-dependent (BOLD) resting-state functional MRI (rsfMRI) datasets (Materials and Methods, Data Analysis), we identified 87 functional components, the patterns of which covered neur...