ObjectiveTrigeminal neuralgia (TN), one of the most severe and debilitating chronic pain conditions, is often accompanied by mood disorders, such as anxiety and depression. Electroacupuncture (EA) is a characteristic therapy of Traditional Chinese Medicine with analgesic and anxiolytic effects. This study aimed to investigate whether EA ameliorates abnormal TN orofacial pain and anxiety-like behavior by altering synaptic plasticity in the hippocampus CA1.Materials and methodsA mouse infraorbital nerve transection model (pT-ION) of neuropathic pain was established, and EA or sham EA was used to treat ipsilateral acupuncture points (GV20-Baihui and ST7-Xiaguan). Golgi–Cox staining and transmission electron microscopy (TEM) were administrated to observe the changes of synaptic plasticity in the hippocampus CA1.ResultsStable and persistent orofacial allodynia and anxiety-like behaviors induced by pT-ION were related to changes in hippocampal synaptic plasticity. Golgi stainings showed a decrease in the density of dendritic spines, especially mushroom-type dendritic spines, in hippocampal CA1 neurons of pT-ION mice. TEM results showed that the density of synapses, membrane thickness of the postsynaptic density, and length of the synaptic active zone were decreased, whereas the width of the synaptic cleft was increased in pT-ION mice. EA attenuated pT-ION-induced orofacial allodynia and anxiety-like behaviors and effectively reversed the abnormal changes in dendritic spines and synapse of the hippocampal CA1 region.ConclusionEA modulates synaptic plasticity of hippocampal CA1 neurons, thereby reducing abnormal orofacial pain and anxiety-like behavior. This provides evidence for a TN treatment strategy.
This study aimed to examine the spontaneous hemodynamic fluctuations and the dysfunctional brain regions in patients with generalized anxiety disorder (GAD) using resting-state functional MRI. Previous studies have demonstrated some neural networks that are different in this patient group compared with healthy controls. However, there is still a need for precise anatomical localization of the aberrantly operating networks. We used resting-state functional MRI to measure the hemodynamic fluctuations in 31 GAD patients and 31 control participants matched for sex, age, and education. On the basis of the hemodynamic fluctuations, we calculated regional homogeneity (ReHo) for our comparisons as this measure reflects coherent fluctuations in adjacently located brain regions. The Hamilton Anxiety Rating Scale was used to assess symptom severity of the GAD patients. There were no significant differences with respect to age, sex, handedness, and education. However, compared with controls, GAD patients showed higher Hamilton Anxiety Rating Scale scores (16.90±1.94, P<0.05). We identified decreased ReHo measures in the right inferior frontal gyrus and the left caudate nucleus in the GAD group compared with the healthy controls. In addition, we found increased ReHo measures within the left cingulate gyrus. This study further complements the network characteristics in anxiety patients and presents new and more accurate anatomical positioning about GAD patients.
Neuropathic pain is mainly triggered after nerve injury and associated with plasticity of the nociceptive pathway in primary sensory neurons. Currently, the treatment remains a challenge. In order to identify specific therapeutic targets, it is necessary to clarify the underlying mechanisms of neuropathic pain. It is well established that primary sensory neuron sensitization (peripheral sensitization) is one of the main components of neuropathic pain. Calcium channels act as key mediators in peripheral sensitization. As the target of gabapentin, the calcium channel subunit α2δ1 (Cavα2δ1) is a potential entry point in neuropathic pain research. Numerous studies have demonstrated that the upstream and downstream targets of Cavα2δ1 of the peripheral primary neurons, including thrombospondins, N-methyl-D-aspartate receptors, transient receptor potential ankyrin 1 (TRPA1), transient receptor potential vanilloid family 1 (TRPV1), and protein kinase C (PKC), are involved in neuropathic pain. Thus, we reviewed and discussed the role of Cavα2δ1 and the associated signaling axis in neuropathic pain conditions.
Despite extensive research in recent decades, knowledge of the pathophysiology of depression in neural circuits remains limited. Recently, the lateral habenula (LHb) has been extensively reported to undergo a series of adaptive changes at multiple levels during the depression state. As a crucial relay in brain networks associated with emotion regulation, LHb receives excitatory or inhibitory projections from upstream brain regions related to stress and cognition and interacts with brain regions involved in emotion regulation. A series of pathological alterations induced by aberrant inputs cause abnormal function of the LHb, resulting in dysregulation of mood and motivation, which present with depressive-like phenotypes in rodents. Herein, we systematically combed advances from rodents, summarized changes in the LHb and related neural circuits in depression, and attempted to analyze the intrinsic logical relationship among these pathological alterations. We expect that this summary will greatly enhance our understanding of the pathological processes of depression. This is advantageous for fostering the understanding and screening of potential antidepressant targets against LHb.
Objective To evaluate whether migraine without aura (MwoA) can be partly attributed to abnormalities of vision-related brain networks (VBN) and whether these specific regional abnormalities affect the patients’ quality of life (QoL). Methods A total of 40 participants, including 20 MwoA patients and 20 healthy control volunteers, were enrolled. There were no significant differences in sex, age, educational qualifications and dominant hand between the two groups. Headache intensity and QoL were assessed by the Pain Number Evaluation Scale (NRS) and the Migraine-Specific Quality of Life Questionnaire (MSQ 2.1), respectively. Resting state functional magnetic resonance imaging (rs-fMRI) and independent component analysis (ICA) were performed to determine and evaluate the VBN. Results Three components were identified as consistent with the VBN in the template and recorded as N1, N2 and N3, respectively. The functional activity of the left primary visual cortex (N1), left culmen of cerebellum (N1), left lingual gyrus (N2), superior frontal gyrus (N2) and left posterior lateral prefrontal cortex (N3) in the MwoA group enhanced compared with the healthy control group. However, the functional activity of right middle occipital gyrus, left fusiform gyrus, right lingual gyrus, and right primary motor cortex in the N3 network weakened. Pearson correlation analysis showed that decline of attention to work and life (MSQ5) was positively associated with the functional activity of left primary visual cortex and left lingual gyrus. Canceling from work and daily life (MSQ8) was inversely associated with the functional activity of right primary motor cortex. The burden of feeling like others (MSQ13) and the overall decrease in QoL were both positively associated with the functional activity of right lingual gyrus. Conclusion MwoA patients showed abnormal VBN function, which was moderately correlated with decreased QoL. This study provides evidence for the precise prevention and treatment of migraine by neural regulation.
IntroductionMultiple sclerosis is an immune-mediated demyelinating disorder of the central nervous system. Because of the complexity of etiology, pathology, clinical manifestations, and the diversity of classification, the diagnosis of MS is very difficult. We found that McDonald Criteria is very strict and relies heavily on the evidence for DIS and DIT. Therefore, we hope to find a new method to supplement the evidence and improve the accuracy of MS diagnosis.ResultsWe finally selected GSE61240, GSE18781, and GSE185047 based on the GPL570 platform to build a diagnosis model. We initially selected 54 MS susceptibility locus genes identified by IMSGC and WTCCC2 as predictors for the model. After Random Forests and other series of screening, the logistic regression model was established with 4 genes as the final predictors. In external validation, the model showed high accuracy with an AUC of 0.96 and an accuracy of 86.30%. Finally, we established a nomogram and an online prediction tool to better display the diagnosis model.ConclusionThe diagnosis model based on microarray data in this study has a high degree of discrimination and calibration in the validation set, which is helpful for diagnosis in the absence of evidence for DIS and DIT. Only one SLE case was misdiagnosed as MS, indicating that the model has a high specificity (93.93%), which is useful for differential diagnosis. The significance of the study lies in proving that it is feasible to identify MS by peripheral blood RNA, and the further application of the model and be used as a supplement to McDonald Criteria still need to be trained with larger sample size.
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