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.

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