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In the DMD rat thalamus, DTI revealed an increase in fractional anisotropy (FA) and a decrease in RD. Smaller normalized brain volume correlated to severity of muscle dystrophy (r = -0.975). Neurochemical changes in the DMD rat brain included increased GABA and NAA in the prefrontal cortex, and GABA in the hippocampus. Such findings could indicate disturbed motor and sensory signaling, resulting in a dysfunctional GABAergic neurotransmission, and an unstable osmoregulation in the dystrophin-null brain.Cervical discogenic pain (CDP) is a clinically common pain syndrome caused by cervical disk degeneration. A large number of studies have reported that CDP results in brain functional impairments. However, the detailed dynamic brain functional abnormalities in CDP are still unclear. In this study, using resting-state functional magnetic resonance imaging, we explored the neural basis of CDP with 40 CDP patients and 40 age-, gender-matched healthy controls to delineate the changes of the voxel-level static and dynamic amplitude of low frequency fluctuations (ALFF). We found increased static ALFF in left insula (INS) and posterior precuneus (PCu), and decreased static ALFF in left precentral/postcentral gyrus (PreCG/PoCG), thalamus (THA), and subgenual anterior cingulate cortex in CPD patients compared to healthy controls. We also found decreased dynamic ALFF in left PreCG/PoCG, right posterior middle temporal gyrus, and bilateral THA. Moreover, we found that static ALFF in left PreCG/PoCG and dynamic ALFF in THA were significantly negatively correlated with visual analog scale and disease duration, respectively. Our findings provide the neurophysiological basis for CDP and facilitate understanding the neuropathology of CDP.DNA hypermethylation has been widely observed in temporal lobe epilepsy (TLE), in which NR4A1 knockdown has been reported to be able to alleviate seizure severity in mouse model, while the underlying methylation-imaging pathway modulated by aberrant methylation levels of NR4A1 remains to be clarified in patients with TLE. Here, using multi-site canonical correlation analysis with reference, methylation levels of NR4A1 in blood were used as priori to guide fusion of three MRI features functional connectivity (FC), fractional anisotropy (FA), and gray matter volume (GMV) for 56 TLE patients and 65 healthy controls. Post-hoc correlations were further evaluated between the identified NR4A1-associated brain components and disease onset. Results suggested that higher NR4A1 methylation levels in TLE were related with impaired temporal-cerebellar and occipital-cerebellar FC strength, lower FA in cingulum (hippocampus), and reduced GMV in putamen, temporal pole, and cerebellum. Moreover, findings were also replicated well in both patient subsets with either right TLE or left TLE only. Particularly, right TLE patients showed poorer cognitive abilities and more severe brain impairment than left TLE patients, especially more reduced GMV in thalamus. In summary, this work revealed a potential imaging-methylation pathway modulated by higher NR4A1 methylation in TLE via data mining, which may impact the above-mentioned multimodal brain circuits and was also associated with earlier disease onset and more cognitive deficits.The aim of this perspective is to propose and discuss the integration of transcranial magnetic stimulation (TMS) over the dorsolateral prefrontal cortex with virtual reality (VR) food exposure for therapeutic interventions for food addiction. "Food addiction" is a dysfunctional eating pattern which is typically observed in eating disorders (ED) such as bulimia nervosa and binge eating disorder. Retin-A Food addiction has been compared to substance use disorder due to the necessity of consuming a substance (food) and the presence of a dependence behavior. In recent years, VR has been applied in the treatment of ED because it triggers psychological and physiological responses through food exposure in place of real stimuli. Virtual reality-Cue exposure therapy has been proven as a valid technique for regulating anxiety and food craving in ED. More, TMS has been proven to modulate circuits and networks implicated in neuropsychiatric disorders and is effective in treating addiction such as nicotine craving and consumption and cocaine use disorder. The combination of a simulative technology and a neurostimulation would presumably provide better improvement compared to a single intervention because it implies the presence of both cognitive and neuropsychological techniques. The possible advantage of this approach will be discussed in the perspective.The consequence of repeated cocaine exposure and prolonged abstinence on glutamate receptor expression in the nucleus accumbens has been extensively studied. However, the early effects of cocaine on NMDAR signaling remain unknown. NMDAR signaling depends on the subunit composition, subcellular localization, and the interaction with proteins at the postsynaptic density (PSD), where NMDARs and other proteins form supercomplexes that are responsible for the signaling pathways activated by NMDAR-induced Ca2+ influx. Here, we investigated the effect of cocaine on NMDAR subunit composition and subcellular localization after both intraperitoneal non-contingent cocaine and response-contingent intravenous cocaine self-administration in mice. We found that repeated cocaine exposure, regardless of the route or contingency of drug administration, decreases NMDAR interactions with the PSD and synaptic lipid rafts in the accumbens shell and dorsal striatum. We provide evidence that cocaine triggers an early redistribution of NMDARs from synaptic to extrasynaptic sites, and that this adaptation has implications in the activation of downstream signaling pathways. Thus, consistent with a loss of NMDAR function, cocaine-induced ERK phosphorylation is attenuated. Because early NMDAR activity contributes to the initiation of lasting addiction-relevant neuroadaptations, these data may hold clues into cellular mechanisms responsible for the development of cocaine addiction.
Attention and perception are strongly biased toward information about oneself compared to information about others. The self-attention network, an integrative theoretical framework for understanding the self-prioritization effects (SPE), proposes that the ventromedial prefrontal cortex (VMPFC), and the posterior superior temporal sulcus (pSTS) are the two nodes responsible for the preferential processing of self-related stimuli, which interact with the attentional control network (associated with the dorsolateral prefrontal cortex, DLPFC), responsible for processing other-related stimuli. So far, neuroimaging studies have provided considerable correlational evidence supporting the self-attention network.

Here we went beyond correlational evidence by manipulating cortical activity using high-definition transcranial direct current stimulation (HD-tDCS), a non-invasive brain stimulation method. We assessed whether anodal and cathodal stimulation of the VMPFC or the DLPFC modulates the processing of self- and other-related stimuli.
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