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1.
Neuroscience Bulletin ; (6): 315-324, 2019.
Artigo em Inglês | WPRIM | ID: wpr-775449

RESUMO

The thalamostriatal pathway is implicated in Parkinson's disease (PD); however, PD-related changes in the relationship between oscillatory activity in the centromedian-parafascicular complex (CM/Pf, or the Pf in rodents) and the dorsal striatum (DS) remain unclear. Therefore, we simultaneously recorded local field potentials (LFPs) in both the Pf and DS of hemiparkinsonian and control rats during epochs of rest or treadmill walking. The dopamine-lesioned rats showed increased LFP power in the beta band (12 Hz-35 Hz) in the Pf and DS during both epochs, but decreased LFP power in the delta (0.5 Hz-3 Hz) band in the Pf during rest epochs and in the DS during both epochs, compared to control rats. In addition, exaggerated low gamma (35 Hz-70 Hz) oscillations after dopamine loss were restricted to the Pf regardless of the behavioral state. Furthermore, enhanced synchronization of LFP oscillations was found between the Pf and DS after the dopamine lesion. Significant increases occurred in the mean coherence in both theta (3 Hz-7 Hz) and beta bands, and a significant increase was also noted in the phase coherence in the beta band between the Pf and DS during rest epochs. During the treadmill walking epochs, significant increases were found in both the alpha (7 Hz-12 Hz) and beta bands for two coherence measures. Collectively, dramatic changes in the relative LFP power and coherence in the thalamostriatal pathway may underlie the dysfunction of the basal ganglia-thalamocortical network circuits in PD, contributing to some of the motor and non-motor symptoms of the disease.


Assuntos
Animais , Masculino , Ondas Encefálicas , Fisiologia , Corpo Estriado , Sincronização Cortical , Fisiologia , Neurônios Dopaminérgicos , Fisiologia , Eletrocorticografia , Vias Neurais , Oxidopamina , Transtornos Parkinsonianos , Ratos Wistar , Núcleos Talâmicos , Caminhada , Fisiologia
2.
Military Medical Sciences ; (12): 957-961, 2014.
Artigo em Chinês | WPRIM | ID: wpr-462467

RESUMO

Objective To investigate the protective effect and the possible mechanism of Wenshen Shengjing Decoction (WSSJD)(including Cornu Cervi Nippon Parvum , Panax ginseng, Cynomorium songaricum, Cistanche deserticola,Radix Astragali, Epimedium brevicornum, Angelica sinensis.) on cyclophosphamide induced testicular oxidative damage in mice . Methods Eight-week-old male Kunming mice were assigned .Mice in normal control group received intraperitoneally nor-mal saline, and mice in Western medicine group ,WSSJD group and model group were injected intraperitoneally with cyclo-phosphamide [80 mg/(kg? d) ]for five days.Then mice in Western medicine group and WSSJD group were gavaged with clomifene citrate or WSSJD for 30 days consecutively .The epididymal sperm count and sperm viability were recorded , and the structure of seminiferous epithelium was observed .The content of malondialdehyde (MDA) and glutathione (GSH), and activities of glutathione peroxidase ( GSH-Px) and catalase ( CAT) in testicular tissue were detected .Immunohisto-chemical technique was used to detect the expression of survivin in spermatogenic cells .The apoptosis of spermatogenic cells in the testes was detected by TUNEL assay .Results Compared with model and Western medicine groups ,the epidid-ymal sperm count and sperm viability rate , the development of seminiferous epithelium , and the activities of GSH-Px and CAT significantly increased , while the MDA content significantly decreased in WSSJD group .The expression of survivin in spermatogenic cells was significantly improved .The apoptotic indexes of seminiferous tubules and spermatogenic cells significantly decreased in WSSJD group .Conclusion These results suggest that WSSJD can significantly improve the impaired reproductive function induced by cyclophospamide in mice by enhancing the antioxidative capability in testes and reducing the apoptosis of spermatogenic cells .

3.
Military Medical Sciences ; (12): 745-747, 2014.
Artigo em Chinês | WPRIM | ID: wpr-459467

RESUMO

Prior to implantation, the blastocyst has to hatch out of its zona pellucida to invade the endometrium .In mammals including humans , failure of blastocyst hatching leads to infertility .Blastocyst hatching is believed to be regulated by a variety of autocrine and paracrine molecules such as proteases , cyclooxygenase-2, p38 mitogen-activated protein ki-nase, activin A and Wnt signal pathway .This article reviews the mechanisms of the key molecular regulators involved in mammalian blastocyst hatching and hatching-assisting methods , which can help clarify the mechanism of blastocyst hatching and the treatment of infertility due to failure in blastocyst hatching .

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