神經(jīng)科學(xué)百科全書(shū):細(xì)胞內(nèi)轉(zhuǎn)運(yùn)與細(xì)胞骨架(英文版)(影印版)(導(dǎo)讀版)
定 價(jià):158 元
- 作者:斯奎爾 ,(Larry.R.Squire) 著
- 出版時(shí)間:2010/8/1
- ISBN:9787030280817
- 出 版 社:科學(xué)出版社
- 中圖法分類:Q2
- 頁(yè)碼:674
- 紙張:膠版紙
- 版次:1
- 開(kāi)本:16開(kāi)
什么是百科全書(shū)?這一名詞來(lái)自于兩個(gè)希臘單詞:enkuklios(意思是循環(huán)的)和paideia(意思是教育)。在16世紀(jì)早期,拉丁手稿的抄寫(xiě)者們將這兩個(gè)單詞合而為一,其在英語(yǔ)中演化為一個(gè)單詞,意思是具有廣泛指導(dǎo)意義的工具書(shū)(The American Heritage Dictionary,2000,Boston:Houghton Mifflin,p.589)。從其來(lái)源可見(jiàn),其希臘文原詞中蘊(yùn)含著以探索、綜合的方式努力獲取知識(shí)的含義。無(wú)論是拉丁文還是英文,該單詞泛指涵蓋廣泛領(lǐng)域知識(shí)的工具書(shū)。
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《神經(jīng)科學(xué)百科全書(shū):細(xì)胞內(nèi)轉(zhuǎn)運(yùn)與細(xì)胞骨架(英文版)(影印版)(導(dǎo)讀版)》書(shū)篇幅巨大,為所有神經(jīng)科學(xué)百科全書(shū)之首。由來(lái)自世界各地的2400多位專家撰稿人合力打造,覆蓋了神經(jīng)科學(xué)全部主要領(lǐng)域。書(shū)中每個(gè)詞條在收入書(shū)中之前均經(jīng)過(guò)顧問(wèn)委員會(huì)的同行評(píng)議,詞條中均含有詞匯表、引言、參考文獻(xiàn)和豐富的交叉參考內(nèi)容。 ·主編為著名神經(jīng)科學(xué)家、美國(guó)神經(jīng)科學(xué)學(xué)會(huì)前主席Larry R Squire。 ·內(nèi)容平易.本科生即可讀性。 ·深度和廣度獨(dú)一無(wú)二,足可滿足專家學(xué)者的需要。 ·導(dǎo)讀版精選啄書(shū)中的部分主題,按內(nèi)容重新編排。更適合讀者購(gòu)買和閱讀。
什么是百科全書(shū)?這一名詞來(lái)自于兩個(gè)希臘單詞:enkuklios(意思是循環(huán)的)和paideia(意思是教育)。在16世紀(jì)早期,拉丁手稿的抄寫(xiě)者們將這兩個(gè)單詞合而為一,其在英語(yǔ)中演化為一個(gè)單詞,意思是具有廣泛指導(dǎo)意義的工具書(shū)(The American Heritage Dictionary,2000,Boston:Houghton Mifflin,p.589)。從其來(lái)源可見(jiàn),其希臘文原詞中蘊(yùn)含著以探索、綜合的方式努力獲取知識(shí)的含義。無(wú)論是拉丁文還是英文,該單詞泛指涵蓋廣泛領(lǐng)域知識(shí)的工具書(shū)。
希臘文中強(qiáng)調(diào)的以創(chuàng)造性手段獲取知識(shí),在神經(jīng)科學(xué)領(lǐng)域尤其適用。神經(jīng)科學(xué)本身就是一個(gè)非常新的名詞。Francis Schmitt在本書(shū)第一版的前言中指出,本書(shū)的編寫(xiě)過(guò)程就是將不同領(lǐng)域的科學(xué)家們聚集在一起,沖擊大腦研究中最頑固的難題。他推動(dòng)建立了神經(jīng)科學(xué)研究項(xiàng)目(Neuroscience Research Program,簡(jiǎn)稱NRP)。早期的NRP成員包括一些學(xué)術(shù)巨匠,如因關(guān)于光合作用的研究獲得諾貝爾獎(jiǎng)的Melvin Calvin、諾貝爾獎(jiǎng)獲得者物理化學(xué)家Manfred Eigen、生物化學(xué)家Albert Lehninger,和當(dāng)時(shí)正在努力破解基因編碼的年輕分子生物學(xué)家Marshall Nirenberg。
細(xì)胞內(nèi)信號(hào)級(jí)聯(lián)與第二信使
Calcium-Calmodulin Kinase II (CaMKII) in Learning and Memory
Cyclic AMP (cAMP) Role in Learning and Memory
Eph Receptor Signaling and Spine Morphology
MAP Kinase Signaling in Learning and Memory
Neural Crest Cell Diversification and Specification: ErbB Role
Notch Pathway: Lateral Inhibition
Notch Signal Transduction: Molecular and Cellular Mechanisms
Retinoic Acid Signaling and Neural Patterning
Sonic Hedgehog and Neural Patterning
Synaptic Plasticity: Diacylglycerol Signalling Role
Wnt Pathway and Neural Patterning
細(xì)胞內(nèi)轉(zhuǎn)運(yùn)與細(xì)胞骨架
Actin Cytoskeleton in Growth Cones, Nerve Terminals, and Dendritic Spines
AMPA Receptor Cell Biology/Trafficking
Axonal and Dendritic Identity and Structure: Control of
Axonal and Dendritic Transport by Dyneins and Kinesins in Neurons
Axonal mRNA Transport and Functions
Axonal Transport and ALS
Axonal Transport and Alzheimers Disease
Axonal Transport and Huntingtons Disease
Axonal Transport and Neurodegenerative Diseases
Axonal Transport Disorders
Axonal Transport Tracers
Cytoskeletal Interactions in the Neuron
Cytoskeleton in Plasticity
Dendrites: Localized Translation
Dendritic RNA Transport: Dynamic Spatio-Temporal Control of Neuronal Gene Expression
Dystrophin, Associated Proteins, and Muscular Dystrophy
Intermediate Filaments
LIM Kinase and Actin Regulation of Spines
Lysosome and Endosome Organization and Transport in Neurons
Microtubule Associated Proteins in Neurons
Microtubules: Organization and Function in Neurons
Mitochondrial Organization and Transport in Neurons
Myosin Transport and Neuronal Function
Neurofilaments: Organization and Function in Neurons
Neuronal Motility and Structure: MARK and GSK Pathways
NMDA Receptors, Cell Biology and Trafficking
Nuclear Movements in Neurons
Peroxisomes: Organization and Transport in Neurons
Prion Transport
Proteasome Role in Neurodegeneration
Protein Folding and the Role of Chaperone Proteins in Neurodegenerative Disease
Retrograde Neurotrophic Signaling
Slow Axonal Transport
Spectrin: Organization and Function in Neurons
Transport Dependent Damage Signaling
Vesicular Sorting to Axons and Dendrites
分泌與囊泡循環(huán)
Active Zone
Botulinum and Tetanus Toxins
Calcium Channel Subtypes Involved in Neurotransmitter Release
Calcium Channels and SNARE Proteins
CIRL/Latrophilins
Clathrin and Clathrin-Adaptors
Complexins
Cysteine-String Proteins (CSPs)
Dynamin
Endocytosis: Kiss and Run
Exocytosis: Ca2+-Sensitivity
Fusion Pore
Large Dense Core Vesicles (LDCVs)
Latrotoxin
Liprins, ELKS, and RIM-BP Proteins
Lysosomal System
Muncl3 and Associated Molecules
Muncl8
Neurexins
Neuroligins
Neurosecretion (Regulated Exocytosis in Neuroendocrine Cells)
Neurotransmitter Release from Astrocytes
Neurotransmitter Release: Synchronous and Asynchronous
NSF and SNAPs
Optical Monitoring of Exo- and Endocytosis
PHR (Pam/Highwire/RPM-l)
Piccolo and Bassoon
Presynaptic Receptor Signaling
Rab3
Rab3A Interacting Molecules (RIMs)
RNA Granules: Functions within Presynaptic Terminals and Postsynaptic Spines
SNAREs
Synapsins
Synaptic Plasticity: Short-Term Mechanisms
Synaptic Vesicle Protein-2 (SV2)
Synaptic Vesicles
Synaptojanin
Synaptotagmins
SynCAMs
Synucleins
Vesicle Pools
Vesicular Neurotransmitter Transporters
Voltage-Gated Calcium Channels
原書(shū)詞條中英對(duì)照表
Though the E(spl) enhancerincludes high-affinity proneural binding sites, highlevels of proneural protein expression in the prospec-tive SOP cannot independently drive E(spl) geneexpression because in the absence of NotchIC, Su(H)functions as part of a repressor complex that ensuresgenes in the E(spl) complex are not expressed. Insurrounding non-SOP cells of the PNC, whereNotch is activated by the SOP cell, NotchIc makesSu(H) function as an activator to drive E(spl) geneexpression.The Complementary Role of Bearded Family Genesin the E(Spl) ComplexThe E(spl) complex also includes non-bHLH genes ofthe Bearded (Brd) family. Their expression is alsoregulated by Notch activation; however, unlike theE(spl) bHLH genes, they do not inhibit proneuralgene expression. Instead, they interfere with Deltafunction by inhibiting Neuralized mediated endocy-tosis of Delta, a step that is essential for effectiveactivation of Notch in the neighboring cell (Figure 2).toestablishment of a central biasing mechanism during