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.
Histological changes were examined in the left ventricular free wall of the heart in 40 rats after ligation of the distal anterior descending coronary artery for 15, 30 minutes and 1, 2, 3, 4, 5, 6 hours. Auto-injection of tracers for light microscopy was used to examine the development of collateral circulation. Morphological changes of the ischemic myocardium were observed by PAS staining and transmission electron microscopy. Fifteen minutes after coronary occlusion, the dye was observed in the vein of the ischemic zone; however, 30 minutes after coronary occlusion, the dye appeared in the capillaries of the outer-third layer.These findings suggested that the collateral circulation becomes functional between 15 and 30 minutes after coronary occlusion. Collateral circulation increased gradually in the capillaries of the ischemic zone. Thirty minutes after coronary occlusion the dye was seen only in the outer-third layer of the left ventricular ischemic zone. One hour after occlusion, the dye appeared in the superficial space and the middle-third layer. Three hours after occlusion, the dye was seen in all layers of the ischemic zone. The dye appeared in the ischemic zone, where myocardium damage was not homogeneous. The positive reaction obtained by PAS staining corresponded with the capillaries, veins and superficial spaces in which the dye was evident.These results suggest that collateral circulation, venural back flow and superficial space flow are able to prevent myocardial infarction in early ischemia. (J Nippon Med Sch 1977 ; 64: 329-336)
Abstract. Rat myocardium was examined by electron microscopy after hydrogen peroxide injection through the tail vein. At the initial stage (1-6 hr after injection of hydrogen peroxide), ultrastructural damages included slight edema of the myocytes, dilation of the sarcoplasmic reticulum, disruption of the myofibrils, interstitial edema and the disappearance of elastin. At the early stage (1-7 days), in addition to the ultrastructural damages of the myocardium in the initial stages, swelling and fusion of mitochondria, irregularly-arranged collagen networks and type III bleb formations were observed. At the later stage (14-28 days), tissue damages had recovered. There was little ultrastructural damage in the normal control myocardium. The relationship between oxygen-derived free radicals and early ischemic or ischemia-reperfusion injury is discussed.
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