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Background: Pain sensitization processing in the central nervous system may be related to endometriosis-associated pain in patients. The purpose of this study was to understand the alterations in the abnormal pain response in central brain areas and explore the central sensitization mechanism of endometriosis-associated pain. Methods: An endometriosis model was established in 40 Sprague-Dawley rats, and the rats underwent pain model assessment through behavioral tests. Twenty Sprague-Dawley rats underwent a sham operation as the control group. Thirteen pain rats and 8 control rats received Rs-fMRI examination to explore the brain functional activity areas, and the regional homogeneity (ReHo) method was used to analyze relevant functional signals among the whole brain. The states of neurons and expression of TRPV1 and NMDRA located in the abnormal ReHo signal brain regions were observed using Nissl staining, qRT-PCR and immunohistochemistry. Results: The rats were divided into a pain group and a control group based on the different syndromes and behavioral assessments. We detected significant enhancement of ReHo signals in the anterior cingulate cortex, hippocampus, and thalamus and a reduction in the ReHo values in the basomedial amygdaloid nucleus (BM) and primary motor cortex (M1) in the pain rat group via Rs-fMRI examination. The number of Nissl bodies and apoptotic neurons was increased; moreover, the volume of neurons increased compensatorily in the cingulate cortex, thalamus and hippocampus in the pain group. TRPV1 and NMDRA were overexpressed in apoptotic neurons in the higher ReHo value brain regions in the endometriosis pain group. Conclusion: These findings suggest that in rats with endometriosis-associated pain, ReHo signal enhancement was observed in the cingulate cortex, thalamus and hippocampus, which may be due to the increase in the number of apoptotic neurons or the compensatory increase in the volume of overactive neurons.

The temporoparietal junction plays key roles in vestibular function, motor-sensory ability, and attitude stability. Conventional approaches to studying the temporoparietal junction have drawbacks, and previous studies have focused on self-motion rather than on vestibular spatial perception. Using transcranial direct current stimulation, we explored the temporoparietal junction’s effects on vestibular-guided orientation for self-motion and vestibular spatial perception. Twenty participants underwent position, motion, and time tasks, as well as functional magnetic resonance imaging scans. In the position task, cathodal transcranial direct current stimulation yielded a significantly lower response in the −6, −7, −8, −9, −10, −11, and −12 stimulus conditions for leftward rotations (P < 0.05). In the time task, the temporal bias for real transcranial direct current stimulation significantly differed from that for sham stimulation (P < 0.01). Functional magnetic resonance imaging showed that cathodal transcranial direct current stimulation suppressed functional connectivity between the temporoparietal junction, right insular cortex, and right supplementary motor area. Moreover, the change in connectivity between the right temporoparietal junction seed and the right insular cortex was positively correlated with temporal bias under stimulation. The above mentioned results show that cathodal transcranial direct current stimulation induces immediate and extended vestibular effects, which could suppress the functional connectivity of the temporoparietal junction and in turn reduce contralateral spatial and temporal perception. The consistent variation in temporal and spatial bias suggested that the temporoparietal junction may be the cortical temporal integrator for the internal model. Moreover, transcranial direct current stimulation could modulate the integration process and may thus have potential clinical applications in vestibular disorders caused by temporoparietal junction dysfunction.

Background: Endometriosis (EM) is a common gynecological disease in women of reproductive age. These patients in approximately 80% suffer the various degree pain. This study will investigate synergistically the mechanism of the higher-position central sensitization and offer a pre-clinical experiment evidence for treatment of various location-EM patients with pain.Methods: Twenty Sprague-Dawley rats were induced three types EM including abdominal EM (n=5), gastrocnemius EM (n=5) and ovary EM group (n=5) and one sham control group (n=5). All groups were measured the pain sensitization by hotplate test, then scanned by the functional magnetic resonance imaging (fMRI). The resting-state fMRI (rs-fMRI) date was analyzed using regional homogeneity (ReHo) approach to find out the abnormal functional activity brain regions. Nissl staining method observed the state of neurons in aberrant ReHo signal brain regions.Results: Rats with EM pain sensitization were increased in abdominal EM and gastrocnemius EM than ovary EM group and sham control. The ReHo value is decreased in gastrocnemius EM in right thalamus and left olfactory tubercle compared with other three groups. The number of neurons was decreased; cavitation around nucleus, and pyknotic homogenous nuclei. Nissl bodies were stained deeply, and the shape was irregular in gastrocnemius EM by Nissl staining in right thalamus. In left olfactory tubercle, there was no significant difference in 4 groups. Conclusions:The thalamus may be the potential key brain region for the central sensitization mechanism of various location-EM pain. The oxidative activation may be weakened in thalamus in gastrocnemius EM group with more severe pain. This finding could lend support for future research on the imageology and pathology of various location-EM pain.