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1.
Acupuncture Research ; (6): 370-374, 2018.
Artículo en Chino | WPRIM | ID: wpr-844446

RESUMEN

OBJECTIVE: To observe the effect of electroacupuncture (EA) on changes of learning-memory ability, psychomotor coordination and anxiety-like behavior of cerebral hypoxic-ischemia (CHI) young rats, so as to explore its protective effect on neurons under hypoxic-ischemic conditions. METHODS: SD rats (aged 7 days) were randomly divided into sham operation (sham, n=12), model (n=11), and EA groups (n=12). In addition, 6 young rats in each group were used for observing the number of dendritic spines after Golgi staining. The CHI model was established by ligation of the left common carotid artery combined with hypoxia in a closed transparent vessel. EA was applied to "Baihui" (GV 20)and "Dazhui" (GV 14) for 20 min, once every other day, for 28 days. The rats' behavior changes were assessed by using rotarod performance (for psychomotor coordination), elevated plus maze (anxiety-like behavior) tests and Morris water maze (learning-memory ability) tests, separately. RESULTS: After modeling, the average escape latency and average escape distance of location navigation test within 70 seconds were significantly increased (P0.05). The density of dendritic spines was significantly lo-wer in the model group than in the sham group (P <0.05), and notably higher in the EA group than in the model group (P<0.05). CONCLUSION: EA can improve the learning-memory ability of CHI young rats, which may be related to its effect in protecting the dendritic spines of CA 1 region of hippocampus from injury.

2.
Journal of Veterinary Science ; : 11-16, 2017.
Artículo en Inglés | WPRIM | ID: wpr-224464

RESUMEN

Mammalian target of rapamycin (mTOR) has an important role in various biological processes in cells. In the present study, we investigated temporal changes in mTOR and phosphorylated-mTOR (p-mTOR) expressions in the rat hippocampal CA1 region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). The mTOR immunoreactivity in the pyramidal neurons and mTOR protein level in the hippocampal CA1 region were markedly decreased at 21 and 28 days after 2VO surgery. However, p-mTOR protein expression was significantly increased at 7 days following CCH but then decreased with time. The results indicate that mTOR and p-mTOR expressions change in the hippocampal CA1 region after 2VO surgery and that reduced expressions of mTOR and p-mTOR may be closely related to the CCH-induced neuronal damage in the hippocampal CA1 region.


Asunto(s)
Animales , Ratas , Fenómenos Biológicos , Región CA1 Hipocampal , Arteria Carótida Común , Demencia Vascular , Mamíferos , Neuronas , Células Piramidales , Sirolimus , Serina-Treonina Quinasas TOR
3.
Acta Anatomica Sinica ; (6): 446-451, 2014.
Artículo en Chino | WPRIM | ID: wpr-455097

RESUMEN

Objective To explore the neuroprotective role of Genistein (GEN) on hippocampal CA1 neurons and the possible mechanism following global cerebral ischemia ( GCI) in rats.Methods Seventy five rats were subjected to global cerebral ischemia ( GCI ) by four-vessel occlusion and randomly divided into five groups , sham, ischemia/reperfusion (I/R), GEN, ICI 182,780 and vehicle groups.Fluoro-Jade B and neuron-specific nuclear-binding protein ( NeuN) staining was used to observe CA 1 neuronal survival .TUNEL was used to detect apoptotic neurons .Spatial learning and memory function of the rats were evaluated by Morris water maze .Results The best dose of neuroprotective role of GEN was 1.0mg/kg body weight.Compared with sham, TUNEL-positive neurons in the hippocampal CA1 region increased significantly in I/R and vehicle groups (P<0.01), while post-treatment with GEN (1.0mg/kg) at 5min after ischemia by tail vein injection decreased markedly (P<0.01).Treatment of 1.0mg/kg GEN markedly attenuated spatial learning and memory deficits of the rats after ischemic insult compared to I /R group.Furthermore, ICI 182,780 significantly abolished the neuroprotective role of GEN (P <0.01).Conclusion The low-dose (1.0mg/kg) GEN significantly attenuates neuronal damage and cognitive deficits following GCI in rats , and the mechanism may be involved in estrogen receptor activity.

4.
Chinese Pharmaceutical Journal ; (24): 590-594, 2012.
Artículo en Chino | WPRIM | ID: wpr-860755

RESUMEN

OBJECTIVE: To study the activity of TQHXD on the learning and memory ability of rats with vascular dementia(VD) and its effects on the content of Ach in cerebral cortex. And to investigate the action mechanism of TQHXD on VD in rats. METHODS: VD model was made by common carotid artery injection of a co-thrombus inducer. The 8-arm radial maze experiment was adopted to evaluate the times of working memory errors and reference memory errors. The changes of the pathological area in hippocampus CA1 were observed by optical microscope. Enzyme-linked immunosorbent assay was used to determine the concentration of Ach in rats cerebral cortex. RESULTS: High and middle dose of TQXHD significantly reduce the times of working memory errors and reference memory errors (P<0.01), definitely improved the anormalies of pathological area in hippocampal CA1, and significantly increased the content of Ach in cerebral cortex (P<0.01). CONCLUSION: TQHXD can significantly ameliorate the learning and memory ability of in VD rats. The mechanism may be related to the improvement of the vertebral body cells anomalies in the hippocampal CA1 region and increasing the content of the Ach in cerebral cortex. Copyright 2012 by the Chinese Pharmaceutical Association.

5.
Chinese Traditional and Herbal Drugs ; (24)1994.
Artículo en Chino | WPRIM | ID: wpr-576876

RESUMEN

Objective To investigate the effects of Panax notoginseng saponins(PNS)on both the excitatory and inhibitory synaptic transmission in the pyramidal neurons in hippocampal CA1 region of rats.Methods Wistar male rats(3—4 weeks)were killed by cervical dislocation and hippocampal slices(400 ?m)were prepared,blind whole-cell voltage-clamp recordings were performed on the CA1 pyramidal cells in hippocampal slices to examine and analyze the effects of PNS(0.05—0.4 g/L)on CA1 afferent fiber-evoked excitatory postsynaptic currents(EPSCs)and inhibitory postsynaptic currents(IPSCs),respectively.Moreover,the Schaffer collateral/commissural pathway was stimulated with paired pulses(interpulse interval was 50 ms)and the paired-pulse facilitation(PPF)was analyzed by EPSC2/EPSC1(P2/P1)ratio.Results PNS(0.1—0.4 g/L)significantly depressed amplitude of EPSCs in neurons in the hippocampal CA1 region(P0.05).Conclusion The inhibitory effect of PNS on EPSCs in hippocampal CA1 pyramidal neurons is not due to the reinforcement of the inhibiting interneurons.It may be a result of direct inhibition on excitatory synaptic transmission.The increasing of P2/P1 ratio after PNS application suggests that PNS depresses the excitatory synaptic transmission by presynaptic mechanism.

6.
Acta Anatomica Sinica ; (6)1955.
Artículo en Chino | WPRIM | ID: wpr-578199

RESUMEN

Objective To explore the effect of androgen on learning and memory ability and neurons in hippocampal CA1 region in senescence accelerated mouse prone strain/8(SAMP8).Methods Thirty 7-month-old male SAMP8 were randomly divided into sham-operation control group,castrated group and androgen replacement therapy after castration group.The dose of testosterone undecanoate(TU) was 37.4mg/(kg?15d).The capability of learning and memory was observed 45 days later through the Morris water maze(MWM) test and the change of neurons in hippocampal CA1 region was detected and analyzed by HE staining,immunohistochemal method and computer pathological image analysis system.Results 1.In the MWM test,the escape latency of castrated group were significantly prolonged(P0.05).2.With HE staining,neurons in hippocampal CA1 region of castrated group were found with diffused vacuolar degeneration,and sparse and disordered cellular arranpement.The cell nucleuses were karyochrome and karyopycnosis.The number and optical density of A? immune positive neurons were markedly higher than those of other groups(P

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