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Study On Motion Sickness Facilitated By Activation Of Medial Prefrontal Cortex Via Vestibular Signals

Posted on:2022-12-13Degree:MasterType:Thesis
Country:ChinaCandidate:Z H ZhangFull Text:PDF
GTID:2494306764452784Subject:Endocrine and Systemic Diseases
Abstract/Summary:PDF Full Text Request
Objective: Motion sickness(MS)is a neurodegenerative vestibular autonomic reflex caused by abnormal stimulation of the vestibular system.Symptoms include nausea,dizziness,vomiting,a pale complexion with cold sweat,lethargy,tiredness and mood changes.MS not only brings travel pain to susceptible people,but also causes symptoms of advanced brain function that can greatly affect aviation,aerospace and navigation operations.Therefore,the neural mechanism of MS occurrence and anti-MS strategies have always been very important research topics in aerospace medicine and military medicine.In this study,morphological immunohistochemistry and immunofluorescence staining were performed on the prefrontal cortex to detect the behavioral changes of the prefrontal cortex lesioned,and to clarify the mechanism of the prefrontal cortex in the occurrence and development of motion sickness.Methods:1.Galvanic was used to stimulate vestibular receptors in rats,and the changes of Fos protein,glutamate-ergic neurons and GABAergic neurons in m PFC region of normal rats and stimulated rats were observed and analyzed by immunofluorescence and immunohistochemistry techniques.2.The changes of Fos protein in m PFC region of normal and rotating rats were observed by immunohistochemical technique through double-axis rotation stimulations,and the activation of m PFC neurons was evaluated.3.The m PFC region of rats was lesioned by electrical damage,and the location of damage was determined by immunohistochemistry.Pica(kaolin and normal diet)and open field test were used to detect the incidence of motion sickness in ratsResults: 1.After galvanic and rotational motion stimulation were observed under the microscope,a large number of oval or brown round nuclei were clearly marked in m PFC.These Fos positive neurons were distributed in all layers except layer I in the full length region of the snout and tail of m PFC,with relatively uniform distribution.In contrast,Fos positive neurons were less expressed in the control group in this region,and scattered Fos positive neurons were also observed in other regions,such as the second motor cortex.After galvanic stimulation,the number of Fos positive neurons in stimulation group and control group was 1053±240.50 and 44.25±3.64,respectively.After rotational motion stimulation,the number of Fos positive neurons in the rotationed group and the control group was 509.80±54.40 and 128.30±7.64 respectively.These morphological results indicated that the number of Fos positive neurons in m PFC increased significantly after vestibular receptor stimulation,suggesting that vestibular signals can activate m PFC neuron activity.2.After galvanic stimulation,it was observed that there were a large number of fusiform glutamate neurons and a large number of Fos positive neurons in m PFC.Compared with the control group,the percentage of double marker between glutamate neurons and Fos was 79.43±2.65% and 2.73±0.77%,respectively.After Galvanic stimulation,there were a large number of scattered GABAergic neurons and circular Fos positive neurons in the m PFC region.Compared with the control group,the percentage of GABAergic neurons and Fos double marker was 11.60±2.89% and 2.37±0.93%,respectively.Compared with glutamate neurons,the percentage of double markers between GABA neurons and Fos was not significantly increased.The results suggest that vestibular information mainly activates excitatory projection neurons in m PFC after vestibular organ stimulation.3.Astrocytes were observed in the damaged m PFC area after electrical lesion.The open field test showed that biaxial rotation could affect the movement ability of animals,and the total distance of 15-minute movement was 3366±334.90 cm and 4411±261cm in the lesioned group and the normal control group,respectively.After rotation,they are1388±173.10 cm and 1672±205.40 cm respectively.After double-axis rotation,daily kaolin intake increased significantly from baseline and peaked on the first day after rotation,then gradually decreased to baseline levels,with a lower peak in the lesioned group than in the control group and a significant net increase.After rotational stimulation,the net increase of kaolin was 0.54±0.15 g in the lesioned group and 0.86±0.16 g in the normal control group.At the same time,normal food intake also reached its lowest point on the first day after rotation,and gradually returned to the baseline level thereafter,which is consistent with kaolin data.A significant decrease in the consumption of 2% sucrose water was observed in both the lesioned group and the control group.After rotary stimulation,sucrose water consumption was 19.88±6.03 g and 39.87±11.38 g in the lesioned group and the normal control group,respectively.Conclusion: 1.The m PFC region receives and processes vestibular signals mediated by glutamate neurons,which is demonstrated by increased Fos expression and the double labeling of Cam KII and Fos.2.m PFC region may play a facilitating role in the occurrence and development of MS.3.GABAergic neurons may also be involved in vestibular signal processing of m PFC.
Keywords/Search Tags:motion sickness, Rats, Prefrontal cortex, Fos, Vestibular system
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