Effects of ginsenoside on brain-derived neurotrophic factor and tyrosine kinase B mRNA expression in the hippocampal formation of aged rats*☆

BACKGROUND： There are a limited number of studies involving the effects of ginsenosides, the active component of ginseng, on expression of hippocampal TrkB mRNA in aged rats.
OBJECTIVE： To observe expression of brain-derived neurotrophic factor （BDNF） and tyrosine kinase B （TrkB） mRNA in the hippocampal formation of aged rats, as well as changes after ginsenoside administrated.
DESIGN, TIME AND SETTING： A randomized, controlled experiment was performed at the Department of Anatomy, College of Basic Medical Sciences, China Medical University in March 2005.
MATERIALS： A total of 39 female, Wistar rats were randomly divided into 3 groups （n = 13 each）： young （3-5 months old）, aged （27 months old）, and ginsenoside group （received 25mg/kg/d ginsenoside in the drinking water between 17 and 27 months of age）.
METHODS： Following anesthesia, the rats were exsanguinated and perfused transcardially with chilled, heparinized, 0.9% saline. The brains were removed and post-fixed in 40 g/L paraformaldehyde/phosphate buffer for 20 minutes, and further incubated in 30% sucrose/phosphate buffer overnight.
MAIN OUTCOME MEASURES： In situ hybridization, immunohistochemistry, and image analysis were used to investigate expression of BDNF and TrkB mRNA in the hippocampal formation. RESULTS： The expression levels of BDNF in the hippocampal CA3 and CA1 of aged rats was significantly less than the young group （t = 2.879, 1.814, 1.984, P 〈 0.05）. BDNF expression was significantly greater in the dentate gyrus of the ginsenoside group, compared with the aging group （t = 1.943, P 〈 0.01）. The expression of TrkB mRNA in the hippocampal CA3, CA1, and dentate gyrus of aged rats was less than the young group （t = 3.540, 3.629, 17.905, P 〈 0.01）. TrkB mRNA expression in the CA3 region and dentate gyrus of the ginsenoside group was significantly greater compared with the aging group （t = 1.293, 3.386, P 〈 0.05, 0.01 ）.
CONCLUSION： BDNF and TrkB mRNA expression in the hipp     

Effect of Qingkailing injection on rat embryonic neuronal apoptosis and mitochondrial membrane potential

INTRODUCTION Hyperacute thrombolytic therapy following cerebral ischemic injury is the best project for recovering cerebral brain flow and saving is- chemic brain tissue. Blood reperfusion transforms brain tissue from ischemia to ischemia/reperfusion (I/R…     

Influence of ginsenoside on expression of brain-derived neurotrophic factor and receptor tyrosine kinase B in the medial septum of aged rats★

BACKGROUND： It has beenshown that ginsenoside, the effective component of ginseng, can enhance expression of choline acetyl transferase, as well as brain-derived neurotrophic factor （BDNF） and its receptor tyrosine kinase B （TrkB）, in cholinergic neurons of the basal forebrain. OBJECTIVE： To qualitatively and quantitatively verify the influence of ginsenoside on expression of BDNF and its receptor, TrkB, in the medial septum of aged rats, and to provide a molecular basis for clinical application. DESIGN~ TIME AND SETTING： A contrast study, which was performed in the Department of Anatomy, China Medical University, and the Department of Anatomy, Shenyang Medical College between December 2005 and May 2007. MATERIALS： Thirty-five, healthy, female, Sprague Dawley rats were selected for this study. Ginsenoside （81% purity） was provided by Jilin Ji＇an Wantai Chinese Medicine Factory; anti-BDNF antibody, anti-TrkB antibody, and their kits were provided by Wuhan Boster Company. METHODS： A total of 35 rats were divided into three groups： young （four months old）, aging （26 months old）, and ginsenoside. Rats in the ginsenoside group were administered ginsenoside （25 mg/kg/d） between 17 months and 26 months. MAIN OUTCOME MEASURES： Immunohistochemistry and in situ hybridization were used to measure expression of BDNF and TrkB in the medial septum of aged rats, and the detected results were expressed as gray values. RESULTS： （1） Qualitative detection： using microscopy, degenerative neurons were visible in the medial septum in the aging group. However, neuronal morphology in the ginsenoside group was similar to neurons in the young group. （2） Quantitative detection： the mean gray value of BDNF-positive and TrkB-positive products in the aging group were significantly higher than in the young group （t = 3.346, 4.169, P 〈 0.01）; however, the mean gray value in the ginsenoside group was significantly lower than in the aging group （t = 2.432, 2.651, P 〈 0.01）. CONCLUS     

Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats**☆

BACKGROUND： In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor （BDNF） can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE： To explore changes in BDNF expression and cognitive function in rats after brain injury. DESIGN, TIME AND SETTING： The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University （China） from July 2007 to July 2008. MATERIALS： A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS： Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney＇s method （n = 24, each group）. A bone window was made in rats from the sham operation group （n = 24）, but no attack was conducted. MAIN OUTCOME MEASURES： At days 1, 2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry （streptavidin-biotin-peroxidase complex method）. Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS： Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups （P 〈 0.05）. CONCLUSION： BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats following i     

Changes in brain-derived neurotrophic factor expression after transplanting microencapsulated sciatic nerve cells of rabbits into injured spinal cord of rats

BACKGROUND: Changes of brain-derived neurotrophic factor (BDNF) expression reflect function of nerve cells; meanwhile, they play a significant role in researching interventions on plerosis of nerve injury. OBJECTIVE: To observe and compare the effects on changes of BDNF expression in rats with spinal cord injury between microencapsulated sciatic nerve cells of rabbits and only transplanting sciatic nerve cells of rabbits. DESIGN: Randomized controlled animal study. SETTING: Medical School of Jiujiang College. MATERIALS: The experiment was carried out in the Medical Science Researching Center, Jiujiang College from May 2004 to May 2006. A total of 90 healthy adult SD rats, weighing 250–300 g, of either gender; and 10 rabbits, weighing 2.0–2.5 kg, of either gender, were provided by Jiangxi Experimental Animal Center. METHODS: Sciatic nerve tissue of rabbits was separated to make cell suspension. After centrifugation, suspension was mixed with 15 g/L alginate saline solution and ejaculated to 20 mmol/L barium chloride saline solution by double-cavity ejaculator. The obtained cell microcapsules were suspended in saline. Rats were randomly divided into microencapsulated group, only suspension group, and only injured group with 30 animals in each group. After anesthesia, T10 spinous process and vertebra lamina of rats in the former two groups were exposed. Spinal cord tissue in 2-mm length was removed from rats by spinal cord right hemi-section. The gelatin sponges with the size of 2 mm × 2 mm × 2 mm were grafted as filing cage, and absorbed 10 μL microencapsulated sciatic nerve cells of rabbit in the microencapsulated group and 10 μL sciatic nerve cells of rabbits in the only suspension group; respectively. No graft was placed in the only injured group. MAIN OUTCOME MEASURES: On the 1st, 3rd, 7th, 14th and 28th days after operation, immunohistochemistry (SABC technique) was used to detect distribution and amount of positive-reactive neurons in BDNF of spinal cord samples which were selected as 2 cm away from the injured surface. RESULTS: All the 90 rats were involved in the final analysis. Masses of brown-yellow particles were found in the microencapsulated group, and most of them were distributed in the spinal cord anterior horn neurons and glial cells. The positive-reactive neuron particles were also found in the white matter and gray matter. On the 3rd, 7th, 14th and 28th days after operation, amount of positive-reactive neurons in BDNF in the microencapsulated group was higher than that in the only injured group (P < 0.01) and only suspension group (P < 0.05). CONCLUSION: After transplanting microencapsulated nerve cell suspension into injured spinal cord of rats, distribution and amount of positive-reactive neurons in BDNF of local samples at injured surface are increased remarkably as compared with those by using tissue cell transplantation.     

MiR-206 decreases brain-derived neurotrophic factor levels in a transgenic mouse model of Alzheimer＇s disease

MicroRNA alterations have been reported in patients with Alzheimer＇s disease （AD） and AD mouse models. We now report that miR-206 is upregulated in the hippocampal tissue, cerebrospinal fluid, and plasma of embryonic APP/PS1 transgenic mice. The increased miR-206 downregulates the expression of brain-derived neurotrophic factor （BDNF）. BDNF is neuroprotective against cell death after various insults, but in embryonic and newborn APP/PS1 mice it is decreased. Thus, a specific microRNA alteration may contribute to AD pathology by downregulating BDNF.     

Facial nucleus up-regulation of brain-derived neurotrophic factor mRNA following electroacupuncture treatment in a rabbit model of facial nerve injury*★

BACKGROUND： The effect of acupuncture treatment on peripheral facial nerve injury is generally accepted. However, the mechanisms of action remain poorly understood. OBJECTIVE： To validate the effect of acupoint electro-stimulation on brain-derived neurotrophic factor （BDNF） mRNA expression in the facial nucleus of rabbits with facial nerve injury, with the hypothesis that acupuncture treatment efficacy is related to BDNE DESIGN, TIME AND SETTING： Peripheral facial nerve injury, in situ hybridization, and randomized, controlled, animal trial. The experiment was performed at the Laboratory of Anatomy, Heilongjiang University of Chinese Medicine from March to September 2005. MATERIALS： A total of 120 healthy, adult, Japanese rabbits, with an equal number of males and females were selected. Models of peripheral facial nerve injury were established using the facial nerve pressing method. METHODS： The rabbits were randomly divided into five groups （n = 24）： sham operation, an incision to the left facial skin, followed by suture; model, no treatment following facial nerve model establishment; western medicine, 10 mg vitamin B1, 50 ug vitamin B12, and dexamethasone （2 mg/d, reduced to half every 7 days） intramuscular injection starting with the first day following lesion, once per day; traditional acupuncture, acupuncture at Ytfeng, Quanliao, Dicang, Jiache, Sibai, and Yangbai acupoints using a acupuncture needle with needle twirling every 10 minutes, followed by needle retention for 30 minutes, for successive 5 days; electroacupuncture, similar to the traditional acupuncture group, the Yifeng （negative electrode）, Jiache （positive electrode）, Dicang （negative electrode）, and Sibai （positive electrode） points were connected to an universal pulse electro-therapeutic apparatus for 30 minutes per day, with disperse-dense waves for successive 5 days, and resting for 2 days. MAIN OUTCOME MEASURES： Left hemisphere brain stem tissues were harvested on post-operative days 7, 14, 21, and     

Transfection of the glial cell line-derived neurotrophic factor gene promotes neuronal differentiation简

Glial cell line-derived neurotrophic factor recombinant adenovirus vector-transfected bone marrow mesenchymal stem cells were induced to differentiate into neuron-like cells using inductive medium containing retinoic acid and epidermal growth factor. Cell viability, micro- tubule-associated protein 2-positive cell ratio, and the expression levels of glial cell line-derived neurotrophic factor, nerve growth factor and growth-associated protein-43 protein in the su- pernatant were significantly higher in glial cell line-derived neurotrophic factor/bone marrow mesenchymal stem cells compared with empty virus plasmid-transfected bone marrow mes- enchymal stem cells. Furthermore, microtubule-associated protein 2, glial cell line-derived neurotrophic factor, nerve growth factor and growth-associated protein743 mRNA levels in cell pellets were statistically higher in glial cell line-derived neurotrophic factor/bone marrow mesen- chymal stem cells compared with empty virus plasmid-transfected bone marrow mesenchymal stem cells. These results suggest that glial cell line-derived neurotrophic factor/bone marrow mesenchymal stem cells have a higher rate of induction into neuron-like cells, and this enhanced differentiation into neuron-like cells may be associated with up-regulated expression of glial cell line-derived neurotrophic factor, nerve growth factor and growth-associated protein-43.     

Role of neuronal nitric oxide synthase (nNOS) in Duchenne and Becker muscular dystrophies – Still a possible treatment modality?

Neuronal nitric oxide synthase (nNOS) is involved in nitric oxide (NO) production and suggested to play a crucial role in blood flow regulation of skeletal muscle. During activation of the muscle, NO helps attenuate the sympathetic vasoconstriction to accommodate increased metabolic demands, a phenomenon known as functional sympatholysis. In inherited myopathies such as the dystrophinopathies Duchenne and Becker muscle dystrophies (DMD and BMD), nNOS is lost from the sarcolemma. The loss of nNOS may cause functional ischemia contributing to skeletal and cardiac muscle cell injury. Effects of NO is augmented by inhibiting degradation of the second messenger cyclic guanosine monophosphate (cGMP) using sildenafil and tadalafil, both of which inhibit the enzyme phosphodiesterase 5 (PDE5). In animal models of DMD, PDE5-inhibitors prevent functional ischemia, reduce post-exercise skeletal muscle pathology and fatigue, show amelioration of cardiac muscle cell damage and increase cardiac performance. However, effect on clinical outcomes in DMD and BMD patients have been disappointing with minor effects on upper limb performance and none on ambulation. This review aims to summarize the current knowledge of nNOS function related to functional sympatholysis in skeletal muscle and studies on PDE5-inhibitor treatment in nNOS-deficient animal models and patients.     

Role of brain-derived neurotrophic factor in wobbler mouse motor neuron disease

Brain-derived neurotrophic factor (BDNF) is neuroprotective for motoneurons undergoing degeneration, including those in natural motor neuron disease (MND) in wobbler mice. To assess the role of BDNF in this model of MND, endogenous BDNF immunoreactivity was analyzed by semiquantitative video-image analysis. Affected cervical spinal cord motoneurons had significantly greater BDNF immunoreactivity compared to motoneurons of healthy littermates (P = 0.01) and affected lumbar spinal cord motoneurons (P = 0.008 at age 4 weeks; P = 0.005 at age 8 weeks). Neuronal nitric oxide synthase (n-NOS) immunocytochemistry revealed increased immunoreactivity in the affected cervical spinal cord motoneurons. Exogenous BDNF treatment partially inhibited the increased NOS activity, as quantitatively measured by nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry. The mean number of NADPH-d(+) motoneurons in the cervical anterior horn decreased from 3.5 +/- 1.2 to 1.5 +/- 1.2 (P = 0.002). The increase in endogenous BDNF immunoreactivity in the affected spinal cord may be compensatory in diseased motoneurons, yet it appears to still be inadequate because exogenous BDNF treatment is required to suppress increased NOS activity in degenerating motoneurons. Our study indicates that BDNF is important in halting nitric oxide (NO)-mediated motor neuron degeneration, which has potential implications for the treatment of neurodegenerative disorders.     

一氧化氮合酶活性与抑郁症的相关性

目的通过对抑郁症患者一氧化氮合酶（NOS）活性进行检测，从而研究和探讨一氧化氮合酶、一氧化氮（NO）与抑郁症之间的关系。方法采用分光光度法检测抑郁症患者治疗前后的一氧化氮合酶NOS及其亚型（结构型cNOS、诱导型iNOS）的活性，并与正常对照组比较。结果抑郁症组的NOS、cNOS活性显著低于正常对照组；治疗组的NOS、cNOS活性高于抑郁症（无显著性），但治疗后缓解组的NOS、cNOS活性均显著高于治疗前。各组iNOS的活性无显著差异。结论抑郁症病人的NOS活性下降，而且主要是结构型cNOS活性下降，经治疗缓解后有所提高。因此，NOS和NO很有可能在抑郁症的发病过程中起着重要作用。     

艾司西酞普兰对抑郁模型大鼠行为学及脑脊液、血清脑源性神经营养因子水平的影响

目的:探讨艾司西酞普兰对慢性应激致抑郁模型大鼠行为学及脑脊液、血清脑源性神经营养因子(BDNF)水平的影响。方法:将Sprague Dawley(SD)雄性大鼠随机分为应激组和非应激组,应激组给予慢性不可预知温和应激(CUMS)刺激8周;刺激4周后根据行为学评估[包括强迫游泳实验(FST)、蔗糖水偏爱实验(SPT)、旷场实验(OFT)]及体质量将抑郁行为大鼠随机分为抑郁模型组和抑郁给药组,非应激组随机分为正常对照组和正常给药组,各组6只。第5周起给予两给药组艾司西酞普兰(10 mg/kg·d)腹腔注射4周。刺激及给药结束后对各组大鼠再次行为学评估并检测脑脊液、血清BDNF水平。结果:CUMS 4周后,与非应激组相比,应激组FST中不动时间显著延长,SPT显著降低,OFT中路程及站立次数显著减少,体质量显著降低(P均0.01);药物干预4周后,与抑郁模型组相比,抑郁给药组FST中不动时间显著缩短,SPT及OFT中总路程显著增加(P均0.05);脑脊液、血清BDNF水平抑郁模型组显著低于正常对照组,抑郁给药显著高于抑郁模型组(P0.05或P0.01)。结论:艾司西酞普兰可改善抑郁大鼠的抑郁行为,提高脑脊液及血清BDNF水平。     

Brain-derived neurotrophic factor and post-stroke depression

Brain-derived neurotrophic factor (BDNF) is well known to play a critical role in cognition. Its role in mood disorders, including post stroke depression (PSD), is also recognized with more evidence surfacing. In patients with PSD, their serum BNDF level is lower than in those without depression. Furthermore, antidepressants could enhance BDNF expression in the brain, resulting in an alleviation of depression symptoms. Such therapeutic effect can be abolished in animals with the BDNF gene deleted. In PSD patients, the presence of stroke may contribute to the development of depression, including affecting the expression of BDNF. However, the mechanisms of BDNF in the development of PSD remain largely unknown. Lower BDNF levels may have existed in some patients before stroke onset, making them vulnerable to develop depressive symptoms. Meanwhile, the hypoxic environment induced by stroke could possibly downregulate BDNF expression in the brain. Current antidepressant treatments are not specific for PSD and there is a lack of treatments to address the linkage between stroke and PSD. This review summarizes the current knowledge of BDNF in PSD. By regulating BDNF expression, a synergistic effect may be achieved when such treatments are applied together with existing antidepressants.     

Expression of brain-derived neurotrophic factor in rat hippocampus following focal cerebral ischemic injury

BACKGROUND： The functional role of brain-derived neurotrophic factor （BDNF） is enhanced following cerebral ischemic injury providing neurons with an important self-protection mechanism in early stage ischemia/hypoxia. OBJECTIVE： To investigate the expression pattern of BDNF in different rat hippocampal regions following focal cerebral ischemic injury. DESIGN, TIME AND SETTING： We performed a comparative and neurobiological study of animals in the Department of Histology and Embryology and the Central Laboratory, Hebei Medical University from March to December 2003. MATERIALS： Forty healthy Sprague Dawley rats were randomly divided into a cerebral ischemia group and a sham operation group, with 20 rats per group. METHODS： In the cerebral ischemia group, we occluded the right middle cerebral artery with a suture, threading it to a depth of 17-19 mm. In the sham operation group, the threading depth was approximately 10mm. MAIN OUTCOME MEASURES： We analyzed the expression of BDNF in different hippocampal regions by immunohistochemical staining of brain sections taken on post-operative days 7, 14, 21 and 30. RESULTS： Sham operation group： We observed a number of a few BDNF-positive cells with light staining in the hippocampal CA1 CA4 regions and dentate gyms. Cerebral ischemia group： compared with the sham operation group, BDNF increased on day 7, significantly increased on day 14, and reached a peak on day 21 （P 〈 0.05）. Furthermore, irnmunologically reactive products were darkly stained, and neurons had long axons. BDNF was particularly highly expressed in the hippocampal CA3 and CA4 regions and dentate gyms. CONCLUSION： Cerebral ischemic injury can damage hippocampal neurons. Neurons can increase their anti-ischemic capacity by increasing BDNF expression in the hippocampal CA3 and CA4 regions and dentate gyms.     

Neuronal nitric oxide synthase polymorphisms in obsessive-compulsive disorder

Background: Obsessive-compulsive disorder (OCD) is a mental disease characterized by recurrent and intrusive thoughts and repetitive behaviours that negatively affect the quality-of-life of the patients. Recent studies have implicated the participation of neuronal nitric oxide in OCD pathogenesis as a neurotransmitter modulator.

Aims: To identify whether variations in neuronal nitric oxide synthase (nNOS) genes may render individuals susceptible to OCD development.

Methods: This study examined nNOS polymorphisms in 100 OCD patients and 121 unrelated healthy controls by polymerase chain reaction and restriction enzyme digestion methods.

Results: nNOS 276 C?+?genotype incidence was significantly higher in OCD patients than controls and conferred a 2-fold increased risk for OCD. No significant differences were observed in frequencies of nNOS 84 genotypes between patients and controls.

Conclusion: This study shows an association between nNOS gene polymorphism and OCD. Exact mechanisms by which nNOS gene variants contribute to OCD pathogenesis need to be further investigated.     

抑郁症患者自杀行为与血清脑源性神经营养因子水平的关系

目的:探讨血清脑源性神经营养因子(BDNF)水平与抑郁症患者自杀行为之间的关系.方法:采用酶联吸附反应方法对有自杀行为的21例抑郁症患者(自杀组)、无自杀行为的52例抑郁症患者(非自杀组)以及80例正常人(对照组)血清的BDNF进行检测,应用汉密尔顿抑郁量表(HAMD)对抑郁症患者的抑郁症状进行评定. 结果:抑郁症患者...     

神经源型一氧化氮合酶C276T基因多态性与抑郁症相关分析

目的测定抑郁症患者抗抑郁剂治疗前后血浆一氧化氮（NO）水平变化,旨在探讨神经源型一氧化氮合酶（nNOS）基因C276T多态性与血浆NO浓度及抑郁症发病相关性。方法采用硝酸盐还原酶法测定正常对照组及抑郁症患者治疗前后血浆NO水平;全部受试者取全血标本提取基因组DNA,并采用PCR-RFLP方法对nNOS基因C276T多态性进行基因分型。结果患者组疗前血浆NO水平为（76.8±31.6）μmol/L显著高于疗后[（66.9±25.7）μmol/L,P=0.044]及正常对照组[（64.2±33.3）μmol/L,P=0.02],两组疗后血浆NO水平相比差异无显著性（P=0.588）;根据PCR-RFLP结果,nNOS基因可见两种等位基因条带C、T,组成三种基因型CC、CT、TT,两组等位基因及基因型分布频率差异无显著性（均P〉0.05）,且携带不同基因型者之间血浆NO水平差异亦无显著性（均P〉0.05）。结论血浆NO浓度增高可能是抑郁症发病的影响因素;nNOS基因C276T多态性可能不直接影响血浆NO浓度,也不是抑郁症发病的主要基因因素。     

神经元型一氧化氮合酶的神经生物学研究进展(英文)

神经元型一氧化氮合酶(neuronal nitric oxide synthase,nNOS)主要表达于神经元,在星形胶质细胞和神经干细胞中也有一定水平的表达。不同的mRNA拼接形式产生了nNOS蛋白的5种亚型,包括nNOS- 、nNOS- 、nNOS- 、nNOS- 和nNOS-2。nNOS单体不具催化活性,二聚体是其活性形式。nNOS单体发生二聚化需要四氢生物蝶呤、血红素以及L-精氨酸的结合。nNOS的表达在很大程度上依赖于cAMP反应元件结合蛋白的活化,其催化活性的调节与热休克蛋白90/ 热休克蛋白70、钙调节蛋白、PIN 蛋白,以及自身Ser847和Ser1412位点的磷酸化和脱磷酸化相关。能与nNOS相互作用的蛋白主要有9种,包括突触后密度蛋白95(post-synaptic density protein 95, PSD95)、CALM、CAMKIIA、DLG4、DLG2、PFK-M、CAPON、syntrophin和dynein轻链。其中 PSD95、CAPON和PFK-M是神经元中最重要的 nNOS 调节蛋白。PSD95与nNOS 的相互作用能介导突触形成,并参与N-甲基-D-天冬氨酸诱导的神...     

慢性锂处理对大鼠海马NOS表达的影响

目的　 探讨不同浓度氯化锂对大鼠海马一氧化氮合酶 (NOS)活性和神经元型一氧化氮合酶 (nNOS)蛋白表达的影响 ,阐明锂对学习记忆的影响与NOS表达的关系。方法　将大鼠随机分为对照 (Cont)组和四个氯化锂(LiCl) (3,30 ,30 0 ,30 0 0mg/kg)组 ,分别给予普通饲料和含LiCl(3,30 ,30 0 ,30 0 0mg/kg)的饲料喂养 6 0d ,通过Y -迷宫实验 ,比较各组大鼠学习记忆能力的差别 ;采用黄递酶 (NADPH d)组织化学染色和ABC免疫组织化学染色方法观察各组大鼠海马CA1区、CA3区和齿状回 (DG)一氧化氮合酶 (NOS)与nNOS阳性细胞数的差别。 结果　3,30mg/kgLiCl组大鼠Y 迷宫实验成绩明显好于正常对照组 (P <0 .0 1) ;30 0 ,30 0 0mg/kgLiCl组大鼠则明显差于对照组 (P <0 .0 5 )。NADPH d和ABC免疫组织化学染色结果示 :LiCl(3,30mg/kg)组大鼠海马NOS与nNOS阳性细胞数明显多于Cont组 (P <0 .0 5 ) ;LiCl(30 0 ,30 0 0mg/kg)组大鼠NOS与nNOS阳性细胞数少于Cont组 ,差异有显著性 (P <0 .0 5 )。 结论　 较低浓度的氯化锂能提高大鼠的学习记忆能力 ,增强NOS活性和nNOS蛋白表达 ,而较高浓度的锂则可能减低大鼠学习记忆能力 ,降低NOS活性和nNOS蛋白表达。