In JoVE (1)
Other Publications (8)
- Trends in Endocrinology and Metabolism: TEM
- Proceedings of the National Academy of Sciences of the United States of America
- The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
- Se Pu = Chinese Journal of Chromatography / Zhongguo Hua Xue Hui
- The Journal of Physiology
- Nature Neuroscience
Articles by Haijiang Cai in JoVE
鼠标肾上腺嗜铬细胞分离 Aaron Kolski-Andreaco1, Haijiang Cai2,3, D. Spencer Currle4, K. George Chandy1, Robert H. Chow2,3 1Department of Physiology and Biophysics, University of California, Irvine (UCI), 2Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, 3Zilkha Neurogenetic Institute, University of Southern California, Keck School of Medicine, 4Department of Developmental and Cell Biology, University of California, Irvine (UCI) 肾上腺髓质嗜铬细胞培养系统，在体外设置为激发分泌耦合研究是非常有用的。该协议说明了用于解剖肾上腺然后隔离剥离肾上腺皮质髓质地区的方法。髓质消化成单个的嗜铬细胞，然后证明。
Other articles by Haijiang Cai on PubMed
著述二 Ca2 + 中的积极作用-通过促进囊泡启动触发胞吐。 Proceedings of the National Academy of Sciences of the United States of America. Dec, 2008 | Pubmed ID: 19033464 网罗介导胞是一个多级的突触传递和激素释放的核心过程。Complexins (指挥所） 是绑定非常迅速和复杂，网罗核心高亲和力那里都有提出最近的夹紧复杂和抑制膜融合抑制胞的小蛋白。然而，其他几项研究也表明指挥所的神经递质释放积极监管机构。因此，是否指挥所胞的正面或负面的监管机构是不详，很少泡生命周期阶段中，它们的功能。在这里，我们有系统地剖析了导致胞哺乳动物模型系统中采用挖空救援这一战略的囊泡阶段。我们显示肾上腺嗜铬细胞从 CPX 二敲除小鼠展览大大下降可拆除的泡池 （包括慢慢地随时可调整的池），同时在融合毛孔扩张或形态囊泡对接动力学显示没有变化。表达的 WT CPX 二-但不是的圈套器绑定缺突变体-还原的大小可调整池挖空细胞和 WT 细胞，它显著放大他们。我们的研究结果显示指挥所规管引的泡池的大小，并在 Ca(2+) 触发胞中有了积极的作用。
慢性尼古丁有选择性地提高了 Alpha4beta2 * 烟碱型乙酰胆碱受体黑质纹状体多巴胺通路。 The Journal of Neuroscience : the Official Journal of the Society for Neuroscience. Oct, 2009 | Pubmed ID: 19812319 这些电生理实验，在切片和完好的动物，研究对功能的 alpha4beta2 * nAChRs 黑质纹状体多巴胺 (DA) 能通路中尼古丁在体内长期接触的影响。野生型和 alpha4 烟碱型乙酰胆碱受体 （nAChR） 亚基基因敲除鼠作了录音。慢性尼古丁增强 methyllycaconitine 柠檬酸水合物耐、 二氢-β-erythroidine 氢溴酸敏感烟碱电流诱发 3-1000年妈妈 ACh 安基神经元的黑质帕尔网脉 （信噪比），但不是在 DA 神经元的黑质致密 (SNc)。此增强功能导致更高的信噪比安基神经元的烧成率，并因此增加安基的 SNc DA 神经元的抑制作用。背侧纹状体，功能 alpha4 * nAChRs 神经元的胞体 ； 上没有找到然而，尼古丁行为通过 alpha4beta2 * nAChRs 在 DA 码头调节到中期多刺神经元谷氨酸释放。慢性尼古丁也增加的数量和/或这些 alpha4beta2 * nAChRs 函数。这些数据表明在黑质纹状体 DA 通路，alpha4beta2 * nAChRs 慢性尼古丁增强显示在单元格中键入和 nAChR 子以及细胞隔离舱中的选择性。这些选择性的事件增加的 SNc DA 神经元的信噪比安基神经元抑制作用和还脾气背侧纹状体谷氨酸释放。影响可能减少的 SNc DA 神经元兴奋毒性危险，期间 DA 系统的退行性变也可能抵消提高皮质纹状谷氨酸能投入的效力。这些过程可能有助于烟草使用与帕金森病的逆相关性。
盖茨条件恐惧杏仁核微电路的遗传剖析。 Nature. Nov, 2010 | Pubmed ID: 21068836 不同杏仁核 (神经解剖分支机构) 的处理巴甫洛夫条件的恐惧进行了广泛研究，但这些原子核内异构的神经元子类型的函数的作用仍然知之甚少。在这里我们使用分子遗传方法映射功能连通性亚群的含有 GABA 的神经元，位于中央杏仁核 （CEl），横向细分的表达蛋白激酶 C-δ (PKC δ）。杏仁切片和细胞特异性病毒跟踪中的映射的离子 2 辅助电路指示 PKC-δ(+) 神经元抑制输出神经元的内侧中央杏仁核 (CEm) 和也在 CEl 作出与 PKC-δ(-) 神经元相互抑制神经突触。电气沉默 PKC-δ(+) 神经元在体内的建议它们对应于生理上已确定的单位，均由条件刺激，被称为 CEl(off) 单位有抑制作用。这种对应关系，以及行为的数据，定义中盖茨 CEm 输出控制的水平取决于冻结的 CEl 抑制微电路。
[Determination of Eight Pesticide Residues in Tea by Liquid Chromatography-tandem Mass Spectrometry and Its Uncertainty Evaluation] Se Pu = Chinese Journal of Chromatography / Zhongguo Hua Xue Hui. Sep, 2012 | Pubmed ID: 23285969 A method was developed for the determination of eight pesticide residues (fipronil, imidacloprid, acetamiprid, buprofezin, triadimefon, triadimenol, profenofos, pyridaben) in tea by liquid chromatography-tandem mass spectrometry. The sample was extracted by accelerated solvent extraction with acetone-dichloromethane (1:1, v/v) as solvent, and the extract was then cleaned-up with a Carb/NH2 solid phase extraction (SPE) column. The separation was performed on a Hypersil Gold C, column (150 mm x 2. 1 mm, 5 microm) and with the gradient elution of acetonitrile and 0. 1% formic acid. The eight pesticides were determined in the modes of electrospray ionization (ESI) and multiple reaction monitoring (MRM). The analytes were quantified by matrix-matched internal standard method for imidacloprid and acetamiprid, by matrix-matched external standard method for the other pesticides. The calibration curves showed good linearity in 1 - 100 microg/L for fipronil, and in 5 -200 microg/L for the other pesticides. The limits of quantification (LOQs, S/N> 10) were 2 p.g/kg for fipronil and 10 microg/kg for the other pesticides. The average recoveries ranged from 75. 5% to 115.0% with the relative standard deviations of 2.7% - 7.7% at the spiked levels of 2, 5, 50 microg/kg for fipronil and 10, 50, 100 microg/kg for the other pesticides. The uncertainty evaluation for the results was carried out according to JJF 1059-1999 "Evaluation and Expression of Uncertainty in Measurement". Items constituting measurement uncertainty involved standard solution, weighing of sample, sample pre-treatment, and the measurement repeatability of the equipment were evaluated. The results showed that the measurement uncertainty is mainly due to sample pre-treatment, standard curves and measurement repeatability of the equipment. The method developed is suitable for the conformation and quantification of the pesticides in tea.
Complexin Facilitates Exocytosis and Synchronizes Vesicle Release in Two Secretory Model Systems The Journal of Physiology. May, 2013 | Pubmed ID: 23401610 Complexins (Cplxs) are small, SNARE-associated proteins believed to regulate fast, calcium-triggered exocytosis. However, studies have pointed to either an inhibitory and/or facilitatory role in exocytosis, and the role of Cplxs in synchronizing exocytosis is relatively unexplored. Here, we compare the function of two types of complexin, Cplx 1 and 2, in two model systems of calcium-dependent exocytosis. In mouse neuromuscular junctions (NMJs), we find that lack of Cplx 1 significantly reduces and desynchronizes calcium-triggered synaptic transmission; furthermore, high-frequency stimulation elicits synaptic facilitation, instead of normal synaptic depression, and the degree of facilitation is highly sensitive to the amount of cytoplasmic calcium buffering. In Cplx 2-null adrenal chromaffin cells, we also find decreased and desynchronized evoked release, and identify a significant reduction in the vesicle pool close to the calcium channels (immediately releasable pool, IRP). Viral transduction with either Cplx 1 or 2 rescues both the size of the evoked response and the synchronicity of release, and it restores the IRP size. Our findings in two model systems are mutually compatible and indicate a role of Cplx 1 and 2 in facilitating vesicle priming, and also lead to the new hypothesis that Cplxs may synchronize vesicle release by promoting coupling between secretory vesicles and calcium channels.
Central Amygdala PKC-δ(+) Neurons Mediate the Influence of Multiple Anorexigenic Signals Nature Neuroscience. Sep, 2014 | Pubmed ID: 25064852 Feeding can be inhibited by multiple cues, including those associated with satiety, sickness or unpalatable food. How such anorexigenic signals inhibit feeding at the neural circuit level is not completely understood. Although some inhibitory circuits have been identified, it is not yet clear whether distinct anorexigenic influences are processed in a convergent or parallel manner. The amygdala central nucleus (CEA) has been implicated in feeding control, but its role is controversial. The lateral subdivision of CEA (CEl) contains a subpopulation of GABAergic neurons that are marked by protein kinase C-δ (PKC-δ). We found that CEl PKC-δ(+) neurons in mice were activated by diverse anorexigenic signals in vivo, were required for the inhibition of feeding by such signals and strongly suppressed food intake when activated. They received presynaptic inputs from anatomically distributed neurons activated by different anorexigenic agents. Our data suggest that CEl PKC-δ(+) neurons constitute an important node that mediates the influence of multiple anorexigenic signals.
Ventromedial Hypothalamic Neurons Control a Defensive Emotion State ELife. 2015 | Pubmed ID: 25748136 Defensive behaviors reflect underlying emotion states, such as fear. The hypothalamus plays a role in such behaviors, but prevailing textbook views depict it as an effector of upstream emotion centers, such as the amygdala, rather than as an emotion center itself. We used optogenetic manipulations to probe the function of a specific hypothalamic cell type that mediates innate defensive responses. These neurons are sufficient to drive multiple defensive actions, and required for defensive behaviors in diverse contexts. The behavioral consequences of activating these neurons, moreover, exhibit properties characteristic of emotion states in general, including scalability, (negative) valence, generalization and persistence. Importantly, these neurons can also condition learned defensive behavior, further refuting long-standing claims that the hypothalamus is unable to support emotional learning and therefore is not an emotion center. These data indicate that the hypothalamus plays an integral role to instantiate emotion states, and is not simply a passive effector of upstream emotion centers.