Human brain functional networks contain a few densely connected hubs that play a vital role in transferring information across regions during resting and task states. However, the relationship of these functional hubs to measures of brain physiology, such as regional cerebral blood flow (rCBF), remains incompletely understood. Here, we used functional MRI data of blood-oxygenation-level–dependent and arterial-spin–labeling perfusion contrasts to investigate the relationship between functional connectivity strength (FCS) and rCBF during resting and an N -back working-memory task. During resting state, functional brain hubs with higher FCS were identified, primarily in the default-mode, insula, and visual regions. The FCS showed a striking spatial correlation with rCBF, and the correlation was stronger in the default-mode network (DMN; including medial frontal-parietal cortices) and executive control network (ECN; including lateral frontal-parietal cortices) compared with visual and sensorimotor networks. Moreover, the relationship was connection–distance dependent; i.e., rCBF correlated stronger with long-range hubs than short-range ones. It is notable that several DMN and ECN regions exhibited higher rCBF per unit connectivity strength (rCBF/FCS ratio); whereas, this index was lower in posterior visual areas. During the working-memory experiment, both FCS–rCBF coupling and rCBF/FCS ratio were modulated by task load in the ECN and/or DMN regions. Finally, task-induced changes of FCS and rCBF in the lateral-parietal lobe positively correlated with behavioral performance. Together, our results indicate a tight coupling between blood supply and brain functional topology during rest and its modulation in response to task demands, which may shed light on the physiological basis of human brain functional connectome.

The default mode network (DMN) in humans has been suggested to support a variety of cognitive functions and has been implicated in an array of neuropsychological disorders. However, its function(s) remains poorly understood. We show that rats possess a DMN that is broadly similar to the DMNs of nonhuman primates and humans. Our data suggest that, despite the distinct evolutionary paths between rodent and primate brain, a well-organized, intrinsically coherent DMN appears to be a fundamental feature in the mammalian brain whose primary functions might be to integrate multimodal sensory and affective information to guide behavior in anticipation of changing environmental contingencies.

Synchronized low-frequency spontaneous fluctuations of the functional MRI (fMRI) signal have recently been applied to investigate large-scale neuronal networks of the brain in the absence of specific task instructions. However, the underlying neural mechanisms of these fluctuations remain largely unknown. To this end, electrophysiological recordings and resting-state fMRI measurements were conducted in α-chloralose-anesthetized rats. Using a seed-voxel analysis strategy, region-specific, anesthetic dose-dependent fMRI resting-state functional connectivity was detected in bilateral primary somatosensory cortex (S1FL) of the resting brain. Cortical electroencephalographic signals were also recorded from bilateral S1FL; a visual cortex locus served as a control site. Results demonstrate that, unlike the evoked fMRI response that correlates with power changes in the γ bands, the resting-state fMRI signal correlates with the power coherence in low-frequency bands, particularly the δ band. These data indicate that hemodynamic fMRI signal differentially registers specific electrical oscillatory frequency band activity, suggesting that fMRI may be able to distinguish the ongoing from the evoked activity of the brain.

The human brain is topologically organized into a set of spatially distributed, functionally specific networks. Of these networks, the default-mode network (DMN), executive-control network (ECN), and salience network (SN) have received the most attention recently for their vital roles in cognitive functions. However, very little is known about whether and how the interactions within and between these 3 networks would be modulated by cognitive demands. Here, we employed graph-based modularity analysis to identify the DMN, ECN, and SN during an N-back working memory (WM) task and further investigated the modulation of intra- and inter-network interactions at different cognitive loads. As the task load elevated, functional connectivity decreased within the DMN while increased within the ECN, and the SN connected more with both the DMN and ECN. Within-network connectivity of the ventral and dorsal posterior cingulate cortex was differentially modulated by cognitive load. Further, the superior parietal regions in the ECN showed increased internetwork connections at higher WM loads, and these increases correlated positively with WM task performance. Together, these findings advance our understanding of dynamic integrations of specialized brain systems in response to cognitive demands and may serve as a baseline for assessing potential disruptions of these interactions in pathological conditions.

Drug addiction is a chronic, relapsing brain disorder characterized by compulsive drug seeking and taking. As a feature commonly associated with drug addiction, impulsivity is a risk factor for and is worsened by cocaine use.¹ In contrast, compulsive drug use is a cardinal feature of the disease. Both impulsivity and compulsivity are associated with abnormal frontostriatal structures in cocaine users (CUs).² In addition, extensive preclinical literature suggests a critical striatal role in cocaine addiction.^3-9 Within striatum, a progressive change from mostly ventral to more dorsal processing domains occurs concurrent with the gradual development of compulsive drug consumption. For example, following chronic cocaine self-administration, the spatial extent and magnitude of neuronal activity as measured by glucose metabolism expands in an orderly fashion from the ventral striatum (VS) to encompass the dorsal striatum (DS).⁴ Cross-sectional human studies also implicate the striatum in cocaine addiction, as evidenced by striatal activation in response to cocaine administration,^10,11 striatal dopamine changes in response to cocaine cues,¹² and striatal morphometric abnormality in CUs^2,13 and their drug-naive siblings.¹⁴