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课程代码 356.130.1.01
The teaching outline of Neurobiology
本科生双语教学用
神经生物学系
2005-2-28
Chapter 1 Neurotransmitter systems and function: overview 1. Requirements: 1) knowing the concept of neurotransmitter; the classification of neurotransmitters; the structure and environment of neurons; the neurochemistry of neurotransmitters 2) holding the basic action of neurotransmitters; the criteria of neurotransmitters 3) understanding the mechanism of the action of neurotransmitters 2.Contents: 1) Chemical transmission the concept of neurotransmitter; the process of chemical neurotransmission 2) Neurotransmitter classification 3) Neurons structure and environment 4) Neurotransmitter function basic circuitry; the excitatory action of neurotransmitters; the inhibitory action of neurotransmitters; the mechanism of the action of neurotransmitters; neurotransmitter organization and utilization 5) Neurochemistry of neurotransmitters the criteria of neurotransmitters; the presence, subcellular localization, synthesis, release, receptors and degradation of neurotransmitters 3. Key words:
chemical transmission 化学传递 neurotransmitter 神经递质 neuron 神经元 dendrite 树突 axon 轴突 soma 细胞体 synapse 突触 axo-dentritic synapse 轴突-树突突触 axo-axonic synapse 轴突-轴突突触 axo-somatic synapse 轴突-胞体突触 dendro-dendritic synapse 树突-树突突触 excitatory postsynaptic potentials 兴奋性突触后电位 inhibitory postsynaptic potentials 抑制性突触后电位 asymmetric type 1 synapse 非对称1型突触 symmetric type 2 synapse 对称2型突触 neurotransmitter co-existence 神经递质共存
4. Questions: 1) What makes neurons special? 2) What are the features of neurotransmitters? 3) How does a signal move from one neuron to another? 4) What are the actions of neurotransmitters? Chapter 2 Control of Neuronal Activity1. Requirements: 4) knowing the formation of ionic gradients, the role of pumps and the mechanism underlying resting membrane potential; knowing the methods for recording ion channel currents and membrane potentials 5) holding the features of ion channels and types of ion channels; holding types of calcium channels, regulation of calcium channels by neurotransmitters and types of slow potassium channels. 6) Understanding the mechanism underlying action potentials; understanding the role of slow potassium channels in adaptation and the role of calcium channels in plateau and pacemaking, the role of hyperpolarization-activated cation channels in pacemaking; 2.Contents: 1) The resting state of nerve cells the formation of ionic gradients; the role of pumps; the mechanism underlying resting membrane potential 2) Ion channels the features of ion channels;types of ion channels 3) Action potentials the mechanism underlying action potentials 4) Calcium channels and transmitter release types of calcium channels;regulation of calcium channels by neurotransmitters 5) Ion channels affecting the pattern and frequency of action potential discharges types of slow potassium channels; slow potassium channels and adaptation; calcium channels and plateau and pacemaking; hyperpolarization-activated cation channels and pacemaking 6) Recording neuronal activity recording ion channel currents;single-channel and whole-cell current recording; recording membrane potentials 3. Key words: resting membrane potential 静息膜电位 action potential 动作电位 threshold 阈值 after-potential 后电位 after-hyperpolarization 负后电位 after-depolarization 正后电位 ion channels 离子通道 non-gating channels 非门控离子通道 gating channels 门控离子通道 patch clamp 膜片钳 voltage-gated sodium channels 电压门控钠通道 voltage-gated calcium channels 电压门控钙通道 delayed rectifier potassium channels 延迟整流钾通道 ionic gradients 离子递度 calcium-activated channels 钙激活的钾通道 inwardly-rectifying potassium channels
M-channels
adaptation of action potentials
P/Q calcium channels
L calcium channels
T calcium channels
patch clamp
4. Questions: 5) What are the common features of ion channels? 6) How many types of ion channels are there? 7) What are the roles of ion channels? 8) How are the pattern and frequency of action potential discharges regulated? Chapter 3: Neurotransmitter receptors 1. Requirements: 1) Understand the structure, distribution and functional properties of neurotransmitter receptors. 2) Holding the principles of how the action of drugs at neurotransmitter receptors can be studied. 2. Contents: Concept of receptors • Chemical property: - Polypeptides (proteins). - One or more (up to five) polypeptide chains constitute a complete receptor molecule. - Chain length from 100 to over 1000 amino acids per each chain. • Function of receptors: - Main function is signal transduction. -Information from the extracellular space into the cell. -From cell to cell. -Between cell compartments within a cell. • Importance of receptors for the brain function: -The integration of sensory input, past experience, and inborn instinct by central nervous system in the generation of appropriate behavioral activity is only possible because of the specialized properties and diversity of neurotransmitter receptors in the nervous system that mediate signaling between neurons. Identification and classification of neurotransmitter receptors: •Traditional pharmacological identification: -Potency order of agonists: disadvantages. -Affinity of antagonists. • Impact of modern molecular biology: -Cloning of receptors: methods and use in receptor identification and classification. Receptor mechanisms • Ion channel receptors. • G-protein-coupled receptors. Receptor classification in the post-genomic era • Subtle difference in receptor subtypes. • Subtype selective drugs. • Orphan receptors. Ion channel receptors GeneralOnly a few transmitters are used and diversity of effect is achieved by utilizing a diversity of receptors. • Subunit transmembrane topology The 4TM receptors: nAchRs, GABAARs, Glycine receptors… The 3TM receptors: Glutamate receptors. The 2TM receptors: ATP receptors. • Subunit stiochiometry Homomeric receptors. Heteromeric receptors. Expression of receptor subunit composition Nicotinic receptors: • Pentameric structure. • Subunit composition of peripheral (neuromuscular junction, torpedo electroplaque) nicotinic receptors. • Subunit composition of central nicotinic receptors: -The heteromeric a42b23 subtype. - The homomeric a7 subtype. Glycine receptors GABA receptors •Hetero-pentamers •Mediate fast inhibitory synaptic transmission in the CNS •Complex receptor composition -a subunit (a1-a6) -b subunit (b1-b4) -g (4), s, e, p, r (3) •A minimal combination of a b g is required for reproducing features known for the endogenous GABAA receptors. •Binding of two GABA molecules are required for channel opening. •The GABAA channel is selectively permeable to Cl- ions. •Agonist: GABA, Muscimol. •Competitive antagonist: Bicuculline. •Non-competitive antagonists: picrotoxin, TBPS (t-butylbicyclophosphothianate). •Modulators: -benzodiazepines (potentiation of GABA responses, requires γ subunit, used as transquilizers and sleeping pills). -barbituates (also enhances GABA responses, used to treat epilepsy, sleeping disorder, etc.). -Alcohol (increases ion flow upon GABA binding). Why sleeping pill cannot be taken with alcohol… 5-HT3 receptors Glutamate receptors •Kainite receptors: -GluR5-GluR7, KA1, KA2 subunits. •AMPA receptors: -Homomeric or heteromeric composed of GluR1- GluR4 subunits. -Fast kinetics, mediates fast excitatory synaptic transmission in the CNS. -Permeable to Na, K and sometimes Ca ions. •NMDA receptors: -Requires co-agonist Glycine. -Requires one or more members of NR1, NR2, and NR3 subunits for function. -Slow kinetics. -Ca permeable, Asparagine at the site corresponding to AMPAR Q/R site. -Voltage-dependent Mg blockade, requires depolarization for receptor activation at resting membrane potential – coincidence detector, LTP... -Silent synapse. G-protein-coupled receptors: One peptide chain represents the complete receptor molecule. Seven transmembrane domains (7 TMs) connected by three extracellular and three intracellular loops. The N-terminal end is extracellular, the C-terminus is intracellular. Transmembrane topography and tertinary structure Crystallographic study. Cryoelectron microscopic study. Receptor activation •Ligand-binding domain. •G-protein coupling. Gs, activates adenylyl cyclase; Gi, inhibits adenylyl cyclase; Gq, activates phospholipase C; Gt, activates phosphodiesterase; Go, inhibits voltage-dependent Ca and K channels.
•Receptor dimerisation: effect enhancement; desensitization. 7-TM domain receptor families •Rhodopsin-like Family -Ligand binding within transmembrane domains. -Include rhodopsin; Adrenergic R; Monoamine R; Nucleotide R; Odorant R; Chemokines R. •Glucagon/VIP/calcitonin family Ligand binding outside transmembrane domains. -Include Glucagon/VIP/calcitonin Family (+ coupled to AC); Glicagon, GLP-1, -2; Calcitonin; GHRH; CRF; Parathyroid hormone R. •Metabotropic Glutamate & Chemosensor Family -Ligand binding on large extracellullar N-terminal. -Include mGluRs; GABAB R; Calcium sensing receptors; T1R - sweet taste receptors; V2R – pheromone receptors (rodent). Thrombin receptors G-protein-coupled receptors desensitization-Phosphorylation of G-protein-coupled receptors (GRKs). - Arrestin binding. -Receptor internalization. -Homologous and heterologous desensitization Constitutively active receptors Allostery, inverse agonist. Genetic disease 3. Key words: signaling 通讯,信号传(转)导 agonist 激动剂 antagonist 拮抗剂 ligand 配体 affinity 亲和力 radioligand binding technique 放射配体结合技术 patch-clamp 膜片钳 homology screening 同源性筛选 oligonucleotide 寡核苷酸 homogenization 匀浆 elution 洗提 a-bungarotoxin [生化] a-金环蛇毒素 tubocurarine 筒箭毒碱 ion channel receptors 离子通道受体 G-protein-coupled receptors G-蛋白偶联受体 synapse 突触 glutamatergic 谷胺酸能的 presynaptic 突触前的 ionotropic 趋离子的 postsynaptic 突触后的 metabotrophic 趋代谢的 perisynaptic 突触周围的 ligand-gated ion channels 配体门控离子通道 hexamethonium [药]六甲铵(降血压药) mecamylamine [药]梅坎米胺,四甲双环庚胺,盐酸-3-甲基氨基异樟脑烷(一种降压药) erythroidine 刺桐定 strychnine 士的宁,番木鳖碱 barbiturate [化]巴比妥酸盐 neurosteroid 神经甾体 bicuculline 荷包牡丹碱 picrotoxin [药]木防己苦毒素,苦味毒(用作刺激剂) benzodiazepine [化]苯(并)二氮 locus coeruleus 蓝斑 long-term potentiation (LTP) or long-term depression (LTD) 长时程增强(抑制) crystallography 结晶学 cryoelectron microscopy 晶体电子显微成像术 dimerisation 二聚化 glucagons 胰高血糖素 calcitonin 降钙素 allosteric [生化]变构(象)的 Inverse agonist 反向激动剂 precocious puberty 早熟 retinitis pigmentosa 色素性视网膜炎 4. Questions: 1) Please raise an example to describe how a kind of receptor is identified using combined pharmacological and cloning techniques. 2) Please state the structural characteristics of nicotinic receptors at the neuromuscular junction. 3) Please describe the structural characteristics of muscarinic receptors. 4) What is special in the opening of NMDA receptors? 5) Please briefly state homologous desensitization and heterologous desensitization. Chapter 4: Neurotransmitter release1. Requirements: 1) Be familiar with the neurochemical methods used to measure transmitter release. 2) Appreciate how electrophysiological techniques can be used to investigate the release of neurotransmitter at a single synapse and to determine the effects of drugs and toxins on synaptic transmission. 3) Be able to describe key experiments that have investigated the role of vesicles in neurotransmitter release. 4) Understand the role of synaptic proteins in neurotransmitter release. 2. Contents: Measurement of transmitter release Ex vivo estimation of transmitter turnover rateConcept and principle of turnover rate estimation. In vitro techniquesIn situ preparations: measurement of the concentration of transmitter in the efflux of stimulated, perfused nerve/end-organ preparation. Synaptosomes: homogenization preparation; principle of transmitter release study; advantages and disadvantages; application in transmitter release study. Brain slices: advantages: relative integrity of neurons and pathways; application in transmitter release study. In vivo techniques The cortical cup: principle; advantage and importance in the study of freely moving animals. Microdialysis: principle. Advantages: allow for studes in (1) specific brain areas or nuclei; (2) in both conscious and anaesthetized animals; (3) in long-term. Concept of reverse dialysis. Voltametry: principle and application: monoamines and metabolites. Advantage: sensitive in studying rapid, transient change of transmitter release. Biosensors: leech; bioluminescent protein (aequorin); electrodes coated with glucose oxidase or lactate oxidase. Where does the released transmitter come from?Evidence of quantal release: neurocytochemistry and electron microscopy; Electrophysiology. Transmitter storage vesiclesLarge dense core vesicles (LDCV) and small dense core vesicles (SDCV). Synapsin marker. Release versus storage poolActive zone of synapse. Phosphorylation and dephosphorylation of synapsin in regulation of releasable and reserve pools of vescicles; roles of calcium and CAM kinase. Vescicular exocytosisDocking and fusion: The SNARE hypothesis. Receptor-mediated modulation of Ca-dependent transmitter releaseAutoreceptors-mediated; Heteroreceptors-mediated. Coupling receptors with exocytosisG-protein binding; Ca2+; K+ conductance. Ca++-independet release of neurotransmitterCarrier-mediated release: mechanism of amphetamine induced 5-HT release. Heterocarrier-mediated release 3. Key words: axolemma 轴膜 ex vivo 在体外 in vitro 离体的 in vivo 在体的 turnover rate of neurotransmitter 神经递质清除率 release pool 释放池 reserve pool 贮存池 synaptosome 突触小体 liquid scintillation counting 液闪记数 chromatographic 色谱(分析)的; 色谱法的 the cortical cup 皮层杯 vescicle 囊泡 quantal release 量子释放 chromaffin granules 嗜铬颗粒 freeze-fracture 冰冻蚀刻 large dense core vesicle (LDCV) 致密中心大囊泡 gluteraldehyde 戊二醛 small dense core vesicle (LDCV) 致密中心小囊泡 synapsin 突触素 endocytosis [生](细胞)内吞作用 exocytosis 胞吐作用, 胞吐现象 synaptobrevin 囊泡相关膜蛋白 tetanus [医]破伤风 syntaxin
synaptotagmin
connexin 连接素 autoreceptors 自受体 heteroreceptor 异受体 amphetamine 安非他明,苯丙胺 4. Questions: 1) What is the theoretical assumption on which “turnover rate” is estimated? 2) What are the advantages and disadvantages to study neurotransmitter release in synaptosomes? 3) Please raise the methods you know that can study neurotransmitter release. 4) Please raise the evidence you know that support quantal release of neurotransmitters. 5) Please briefly describe SNARE hypothesis. Chapter 6: Acetylcholine1. Requirements: 1) Master the substrates and sources, enzyme, process, and rate-limiting step in the biosynthesis of acetylcholine. 2) Master the metabolism of Ach. 3) Be familiar with the main distribution of cholinergic receptors and the main subtypes. 4) Understand the functions of central and peripheral cholinergic system. Understand the significance of cholinergic receptors as target of pharmaceutical approaches. 2. Contents: IntroductionDistribution of peripheral cholinergic receptors. Cholinesterase (ChE) and choline acetyltransferase (ChAT) in the mapping of central cholinergic system. Neurochemistry Site and process of the biosynthesis of acetylcholine in cholinergic neurons; source of the substrates; rate-limiting step of the synthesis. High-affinity and low-affinity uptake of choline. Hemicholium and triethylcholine as competitive substrates of choline. Storage and release Labile pool and fixed pool. Mechanism of the toxicity of botulinum toxin and bungarotoxins. Metabolism Breakdown process of acetylcholine; acrtylcholinesterase or specific cholinesterase; butyrylcholinesterase or non-specfic cholinesterase; frequently used Anticholinesterases. Receptors Classificassion and structure Nicotinic receptors: (please refer to Chapter 3). Muscarinic receptors: classification with pharmacological (M1-M5) and molecular (m1-m5) methods; G-protein linkage of different receptor subtypes. Distribution Widespread but of unclear source. Function Nicotinic receptors: Peripheral: Na+-mediated fast neurotransmission (in neuromuscular junction and autonomic ganglions). Central: enhancement of neurotransmission mediated through voltage-gated Ca++ Channels. Muscarinic receptors: excitation of neurons via inhibition of voltage-dependent K+ conductance. Agonists and antagonistsCommon structure and mechanism of action. Drugs and the different muscarinic receptors Cholinergic pathways and functionSpinal cord Neuromuscular junction, feedback circuit of Renshaw cell, receptor subtypes involved. Triatum Highest Ach concentration; intrinsic cholinergic innervation; interaction of Ach and DA system within striaum and the significance of this interaction in Parkinsonism. Cortex Cholinergic subcortical nuclei projecting to the cortex; role of cholinergic pathways in arousal and sleep. Cognition and reward 3. Key words:
neuromuscular junction 神经肌肉接头
sympathetic 交感的
parasympathetic 副交感的
autonomic 自主神经的
leech 水蛭 clam 蛤 cholinesterase 胆碱脂酶 choline acetyltransferase (ChAT) 胆碱乙酰基转移酶 high-affinity uptake 高亲和力摄取 low-affinity uptake 低亲和力摄取 hemicholinium 密胆碱 triethylcholine 三乙基胆碱 labile pool 易变池 botulinum toxin [微]肉毒(杆)菌毒素 botulism 食物中毒 blepharospasm 脸痉挛 cobra 眼镜蛇 interpeduncular 脚间的 caudate 尾核 raphe nucleus 中缝核 acetylcholinesterase [生化]乙酰胆碱酯酶 butyrylcholinesterase [生化]丁酰胆碱酯酶 anticholinesterase [生化]抗胆碱酯酶(如毒扁豆碱) physostigmine [药]毒扁豆碱(一种眼科缩瞳药) neostigmine [药]新斯的明(治疗青光眼等的药) pesticide 杀虫剂 tetrahydro aminoacridine 四氢氨基吖啶 sustantia nigra 黑质 nicotinic [化] 烟碱的, 烟碱酸的 muscarinic 毒蕈碱的 inosotal triphospate 三磷酸肌醇 hippocampus 海马 ventral tegmented area 腹侧顶盖区 carbamyl [化]氨基甲酰 oxotremorine [药]氧化震颤素 methylcarbachol 氨甲基胆碱 carbachol [药]卡巴可,氯化氨甲酰胆碱,碳酰胆碱 suxamethonium (succinylcholine) [药]琥珀胆碱,司可林, 丁二酰胆碱 gallamine: [药]加拉明 pancuronium [药]溴化双哌雄双酯,巴夫龙 (神经肌肉阻滞药或肌松药) decamethonium [药]十烃季铵,十甲季铵,十烷双铵 hyoscine (scopolamine) 东莨菪碱 magnocellular forebrain nucleus (MFN) 巨细胞前脑核 nucleus basalis magnocellularis 基底巨细胞核 substantia innominata 无名质 medial septum 中隔 pontine tegmentum 脑桥被盖 pedunculopontine tegmental nucleus (PPPTN) 脚间脑桥被盖核 laterodorsal tegmental nucleus (LDTN) 背外侧被盖核 ascending reticular system 网状上行系统 rapid eye movement (RAM) sleep 快动相睡眠 lateral geniculate body 外侧膝状体 maze 曲径, 迷宫 amygdala 杏仁核 4. Questions 1) Please describe the process of the biosynthesis of acetylcholine. What is the rate-limiting factor? 2) Please describe the G-protein linkage of muscarinic receptor subtypes. 3) Please describe the fate of the acetylcholine released into the synaptic cleft. 4) What is the neurological mechanism of tetanus? Chapter 7 DOPAMINE1. Requirements: 7) Knowing the methods for detecting dopamine neurons and projection pathways. Knowing the main pathways of dopamine. 8) Holding the main nucleus clusters of dopamine cell bodies. Holding the life cycle of dopamine, including enzymes, transporters and regulation factors. Holding the classification and mechanisms of dopamine receptors. 9) Understanding the synaptic effects and central functions of dopamine. 2.Contents: 1) Pathways of dopamine neurons 2) Neurochemistry of dopamine 2.1 synthesis (enzymes, regulation factors) 2.2 metabolism (enzymes, metabolites) 2.3 storage (vesicular uptake) 2.4 release and reuptake 3) Dopamine receptors 3.1 classification 3.2 distrubution and mechanisms 3.3 agonists and antagonists 4) Synaptic effects 5) Central functions 3. Key words: dopamine (DA) 多巴胺 catecholamine 儿茶酚胺 Substantia nigra 黑质 striatum 纹状体 tyrosine hydroxylase (TH) 酪氨酸羟化酶 dopa decarboxylase (DDC) 多巴脱羧酶 tetrahydropterine 四氢蝶啶 pyridoxal phosphate 磷酸吡哆醛 autoreceptor 自身受体 monoamine oxidase (MAO) 单胺氧化酶 catechol-O-methyl transferase (COMT) 儿茶酚胺氧位甲基移位酶 transporter 转运体 reuptake 重摄取 chemical sympathectomy 交感神经化学切断术 vesicular monoamine transporter (VMAT) 囊泡单胺转运体 Parkinson’s disease 震颤性麻痹, 帕金森氏病 presynaptic 突触前 postsynaptic 突触后 schizophrenia 精神分裂症 psychology 心理学 tardive dyskinesia 迟发性运动障碍 paralysis 麻痹、瘫痪 Chapter 8 NORADRENALINE 1. Requirements: 1) Knowing the methods for detecting noradrenaline neurons and projection pathways. Knowing the main pathways of noradrenaline. 2) Holding the main nucleus clusters of noradrenaline cell bodies. Holding the life cycle of noradrenaline, including enzymes, transporters and regulation factors. Holding the classification and mechanisms of noradrenaline receptors. 3) Understanding the central functions of noradrenaline. 2.Contents: 1) Pathways in CNS 2) Neurochemistry of NA 2.1 Synthesis (enzymes, regulation factors) 2.2 Storage 2.3 Release 2.4 Reuptake 2.5 Metabolism 3) Noradrenergic receptors 3.1 Classification 3.2 Mechanisms 4) Central function 3. Key words: momoamine 单胺 catecholamine 儿茶酚胺 epinephrine (E) 肾上腺素 norepinephrine (NE) 去甲肾上腺素 Retrograde tracing 逆向示踪 cortex 皮层 hippocampus 海马 tyrosine hydroxylase (TH) 酪氨酸羟化酶 dopa decarboxylase (DDC) 多巴脱羧酶 dopamine-b-hydroxylase (DbH) 多巴胺b羟化酶 Vesicular monoamine transporter (VMAT) 囊泡单胺转运体 Transmembrane-spanning domains (TMD) 跨膜域 exocytosis 胞裂外排 reserpine 利血平 chemical sympathectomy 交感神经化学切断术 reuptake 重摄取 locus coeruleus 蓝斑 Chapter 9 5-HYDROXYTRYPTAMINE 1. Requirements: 1) Knowing the methods for detecting 5-HT neurons and projection pathways. Knowing the main pathways of 5-HT. 2) Holding the main nucleus clusters of 5-HT cell bodies. Holding the life cycle of 5-HT, including enzymes, transporters and regulation factors. Holding the classification and mechanisms of 5-HT receptors. 3) Understanding the central functions of 5-HT.
2.Contents: 1) Pathways and distribution in the CNS 2) Neurochemistry of serotonin 2.1 Synthesis (enzymes and regulation factors) 2.2 Storage 2.3 release 2.4 reuptake 2.5 metabolism 3) 5-HT receptors 3.1 classification 3.2 mechanisms 4) Central function 3. Key words: hydroxytryptamine (5-HT)/ serotonin 5-羟色胺 raphe nucleus 中缝核 Indoleamine 吲哚胺 Tryptophan hydroxylase 色氨酸羟化酶 Tricyclic antidepressant 三环类抗抑郁剂 Selective serotonin reuptake inhibitors (SSRIs) 选择性5-HT重摄取抑制剂 depression 抑郁症 4.Questions for Chapter 7,8,9: 1. Please describe the life cycle of one of the monoamine neurotransmitters. 2. Please describe how NA (DA, or 5-HT) are transported from the synaptic cleft to the cytosol and ultimately into the vesicle. 3. Both plasma NA transporter and vesicular monoamine transporter can uptake NA. What is different between the two uptake mechanisms? 4. Tyrosine hydroxylase is the rate-limiting enzyme in NA synthesis. Are there any regulation factors on its activity? 5. Please write down the main enzymes in the metabolism of catecholamine. 6. Please explain where, and how, drugs can interact with the uptake of serotonin. 7. Substantia nigra (locus coeruleus, or raphe nucleus) destruction, which neurotransmitter system will be affected? Chapter 10 Amino acids: excitatory1. Requirements: 1) Understanding the key concepts in excitatory neurotransmission; 2) Knowing the main components of glutamate synapses; 3) Understanding the functional roles of excitatory amino acids; 4) Developing knowledge of related clinical science subjects. 2. Contents: 1) Introduction Major excitatory neurotransmitter: glutamate 2) Neurochemistry of glutamate Glutamate produced from diverse origins 3) Glutamate receptors AMPA and Kainate receptors; NMDA receptors; Metabotropic receptors 4) Functional roles of excitatory amino acids Epilepsy; Pain; Memory; Excitotoxicity; Development 3. Key words: Amino acid neurotransmitters 氨基酸类神经递质 Excitatory 兴奋性 AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazole-proionic acid) a-氨基-3-羟基-5-甲基-4-异噁唑-丙酸 AP5 NMDA受体拮抗剂 Brain ischemia 大脑缺血 7-CK (7 chlorokynureic acid) NMDA受体拮抗剂 CNQX (6-cyano-7-nitroquinoxaline) AMPA受体拮抗剂 Co-existence 共存 CPP (3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid) NMDA受体拮抗剂 Dextrophan 右吗喃,NMDA受体拮抗剂 Epilepsy 癫痫 Exitotoxicity兴奋性毒 Glutamate (L-Glutamic acid) 谷氨酸 Glutamate receptors 谷氨酸受体 Metabotropic 代谢型 Glutamine Synthetase 谷氨酰胺合成酶 Function 功能 Inhibitors 抑制剂 In pain transmission 在痛觉传递中 Kainate (Kainic acid, KA) 红藻氨酸 Kainate receptors 红藻氨酸受体 Ketamine 氯胺酮,NMDA受体拮抗剂 Knock-out mice 基因剔除小鼠 Krebs cycle 三羧酸循环 Memantine 美金刚胺, NMDA受体拮抗剂 MK-801 NMDA受体拮抗剂 MPTP (1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine) 1-甲基-4-苯基-1,2,3,6-四氢吡啶 Neuropathy 神经病 NMDA (N-methyl-D-aspartate) N-甲基-D-天冬氨酸 NMDA receptors NMDA受体 Non-NMDA 非NMDA Noxious stimulus 有害刺激 Parkinson’s Disease (PD) 帕金森氏病 NBQX (6-nitro-7-sulphamoylbenzo(f)quinoxaline-2,3-dione) 2,3-二羟基-6-硝基-7-氨磺酰苯喹喔啉,AMPA受体拮抗剂 Recognition sites 识别位点 Substance P P物质 Synapse 突触 Tachykinins 速激肽 4. Questions: 1) What is the difference between ionotropic and metabotropic neurotransmitter receptors? 2) The structure of the NMDA-receptor complex and explain how it works. 3) Define the terms agonist and antagonist, and provide examples. 4) Explain the excitotoxicity of the glutamate. 5) The main functional roles of glutamate in memory. Chapter 11 Amino acids: inhibitory1. Requirements: 1) Knowing the structures and biosynthesis pathways of the two major inhibitory amino acid neurotransmitters; 2) Understanding the main characteristics of three distinct GABA receptors and GABA transporters; 3) Knowing the main pharmacology of inhibitory neurotransmission; 4) Integrating the knowledge with related clinical science subjects. 2. Contents: 1) Introduction Major inhibitory neurotransmitter: GABA; Glycine 2) Neurochemistry of GABA Synthesis and catabolism; Storage; Uptake; Metabolism 3) GABA receptors (GABAA, GABAB, GABAC) Pharmacology; Structure; Mechanisms 4) Glycine Synthesis and catabolism; Storage; Uptake; Receptors 3. Key words: ACHC (cis-3-aminocyclohexane-carboxylic acid) GABA类似物,GABA再摄取阻断剂 Agonist 激动剂 b-Alanine b-丙氨酸 Allylglycine 烯丙基甘氨酸,GAD竞争性抑制剂 Alphaxalone (3a-hydroxy-5a-pregnan-11,20 dione) a-羟孕双醇,类固醇类 Aminooxyacetic acid GABA-T抑制剂 Antagonists 拮抗剂 Anaesthetics 麻醉剂 APPA (3-aminopropyl phosphinic acid) GABA类似物,GABA受体B激动剂 Baclofen (R-4-amino-3-(4-chlorophenyl)butanoic acid) 氯苯氨丁酸 Barbiturates 巴比妥酸盐 Benzodiazepines苯(并)二氮( 用于制造各种镇静药) Bicuculline 荷包牡丹碱 Binding sites 结合位点 b-Carboline 咔啉,GABA受体拮抗剂 Chloride equilibrium potential 氯离子平衡电位 Complex 复合体 DABA (2,4-diaminobutyric acid) GABA类似物 Diazepam 安定 Distribution 分布 Etomidate 乙醚酯, 麻醉剂 Expression in Xenopus oocytes 在爪蟾卵母细胞中表达 Flumazenil 苯二氮的拮抗剂 GABA (g-aminobutyric acid) g-氨基丁酸 Gabaculine (5-amino-1,3-cyclohexadienenecarboxylic acid) GABA-T抑制剂 GABA receptors g-氨基丁酸受体 GABAA receptors g-氨基丁酸受体A GABAB receptors g-氨基丁酸受体B GABAC receptors g-氨基丁酸受体C GABA-shunt GABA代谢旁路 GABA transaminase (GABA-T) GABA转氨酶 GABAzine GABA受体A拮抗剂 Glutamic acid decarboxylase (GAD) 谷氨酸脱羧酶 Glycine 甘氨酸 Glycine receptors 甘氨酸受体 Glycine transporters 甘氨酸转运蛋白 Guvacine 去甲基槟榔次碱,GABA类似物 Halothane 三氟溴氯乙烷,挥发性麻醉剂 Heterogeneity 异质性 Inhibitory 抑制性 Huntington’s Chorea 亨廷顿氏舞蹈病 Imidazopyridines 咪唑吡啶类,催眠药 Ionotropic 离子型 Isoflurane 异氟醚,挥发性麻醉剂 Isoforms 异构体 Mechanisms of action 作用机制 3-mercaptopropionic acid 3-巯基丙酸,GAD竞争性抑制剂 Metabolism 代谢 Muscimol 蝇覃醇,GABA 受体A激动剂 Neurochemistry 神经化学 Nipecotic acid GABA类似物,GABA再摄取阻断剂 Pharmacology 药理学 Phencyclidine (PCP) 苯环已啶 Picrotoxin 印防己毒素 Presynaptic 突触前 Propanidid 麻醉剂的一种 Propofol 麻醉剂的一种 Purkinje cells 浦肯野氏细胞 Pyridoxal-5-phosphate (PLP) 5-磷酸吡哆醛 Pyridoxamine-5’-phosphate (PMP) 5-磷酸吡哆胺 Quisqualate (Quisqualic acid, Q) 使君子氨酸 Sarcosine (N-methyl glycine) 肌氨酸 Serine hydroxymethyltransferase (SHMT) 丝氨酸羟甲基转移酶 Storage 存储 Structure 结构 Strychnine 的士宁 Sub-units 亚单位 Succinic semialdehyde dehydrogenase (SSADH) 琥珀酸半醛脱氢酶 Succinic semialdehyde reductase (SSAR) 琥珀酸半醛还原酶 Synthesis 合成 Taurine 牛磺酸 TBPS (t-butylbicyclophophorothionate) GABA受体A拮抗剂 THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) 4,5,6,7-四氢异噁唑[5,4-c]-吡啶酮-3-醇 Tricarboxylic acid (TCA) cycle 三羧酸循环 Transporters 转运蛋白 Uptake 摄取 Valproate (2-propylpenatanoic acid) 2-丙基戊酸,GABA-T抑制剂 Vesicular inhibitory amino acid transporter (VIAAT) 小泡型抑制性氨基酸转运蛋白 Vesicular transporters 小泡转运蛋白 Vigabatrin (g-vinyl GABA) 氨己烯酸,GABA-T抑制剂 4. Questions: 1) What is the precursor of the neurotransmitter called GABA? 2) How are EPSP’s and IPSP’s induced in dendrites? How do they change the membrane potential? 3) What is the difference between GABA transporters and vesicular GABA transorter? 4) How does GABAB receptor work? 5) The main process of Glycine neurotransmission. Chap 12 Peptides1. Requirements 1) Understand neuropeptides classification, biosynthesize, release and breakdown; understand neuropeptides receptors and the signal transduction of neuropeptides. 2) Master co-existence of neuropeptides with classical neurotransmitters and function of peptides. 3) Find out Mechanisms of action of opioid peptides 2. Contents 1) Classification of neuropeptides: Opioid peptides, Tachykinins, Cholecystokinin, Neuropeptide Y, Vasopressin, Somatostatin, Neurotensin, CGRP, Galanin 2) Neuropeptids: Biosynthesize, storsge, release and breakdown. 3) Co-existence of neuropeptides with classical neurotransmitters: Comparing with interactions and physiologic significance. 4) Opioid peptides: Receptors; classification; structure-activity relationship; Agonists and Antagonists of opioid receptors; physiologic functions 5) Tachykinin: Characteristic of TK structures; TK receptors, physiologic functions. 6) Cholecystokinin: Characteristic of cholecystokinin; cholecystokinin receptors; physiologic functions. 7) Neuropeptide Y, Somatostatin, Neurotensin, CGRP, Galanin: Structures; receptors; physiologic functions. 3. Key words: neuropeptide 神经肽 post translation processing 翻译后加工 carboxypeptidase 羧肽酶 aminopeptidase 氨肽酶 co-existence 共存作用 synergism 协同作用 antagonism 拮抗作用 inhibition 抑制作用 promotion 促进作用 tachykinin(TK) 速激肽 substance P ( SP) P物质 neuropeptide Y (NP Y) 神经肽Y vasopressin 加压素 calcitonin gene-related peptide (CGRP) 降血钙素基因相关肽 galanin 神经节肽 cholecystokinin (CCK) 胆囊收缩素 pancreozymin (PZ) 促胰液素 gastrin 胃泌素 b-endorphin b-内啡肽 enkephalin 脑啡肽 dynorphins 强啡肽 orphanin 孤啡肽 pre-pro-opiomelanocortin, (POMC) 前孤啡肽原 pre-proenkephalin 前脑啡肽原 leucine-enkephalin (LE) 亮啡肽 methionine-enkephalin (ME) 甲啡肽 lipotropin 趋脂素 somatostatin 生长激素抑制素 neurotensin 神经降压肽 4. Questions 1) What is the neuropeptides? Please illustrate the biosynthesis, storage, release and breakdown of neuropeptide. 2) Recount the interactions and physiologic significance in coexistence of neuropeptides with classical transmitters. 3) Recount the mechanism that CCK reduced the action of morphine analgesia. 4) Specify the relationship between the bioactivity and structure of enkephalin. Chap 13 Other Transmitters and Mediators1. Requirements 1) Understand ATP fulfils the criteria for a NT and the role in the neural control of smooth function. Understand the synthesis, metabolism and receptors of these transmitters. 2) Master the definition of neurosteroids and its characteristic; Master the mechanism of neurosteroid actions. Master the production and actions of NO. 3) Know well the excitotoxicity of NO. 2. Contents 1) The purines, ATP, and adenosine: structures and relationship between adenosine and ATP; synthesis, storage, release, metabolism, receptors, and the mechanism of ATP actions in CNS or PNS; physiological functions. 2) Histamine (HA): synthesis, receptors and its distribution in CNS; physiological functions of HA. 3) Neurosteroids: definition; synthesis and its regulations; correlative receptor and enzymes in synthesis and metabolism of neurosteroids; mechanism of actions; 4) Nitric oxide (NO): Synthesis; cellular actions; pharmacology; function; nociception; Long-term potentiation. 5) Adrenaline, Trypatmine, phenylethylamine, tyramine, Prostaglandins(PGs): synthesis, release and receptors and its functions. 3. Key words Purinergic nerves 嘌呤能神经 adenosine 腺苷 nociceptive 疼痛的,感受伤害的 Convulsant 痉挛 Histamine (HA) 组胺 Hay fever 干草热 mepyramine 美吡胺 promethazine 异丙嗪,抗氨荨 sedation 镇静 Tuberomammillary nucleus 结节乳头核 Limbic areas 边缘区 neurosteroid 神经甾体 genomic effect 基因效应 nongenomic effect 非基因效应 cholesterol 胆固醇 Pregnenolone (PREG) 孕烯醇酮 Progesterone (PROG) 孕酮 allopregnenolone (3a, 5a-ThPROG) 3a, 5a-四氢孕酮 dehydroepiandrosterone (DHEA) 脱氢表雄酮 corticosterone 皮质酮 Vigilance 不眠症,警惕症 adrenaline 肾上腺素 Tryptamine 酪胺 Phenylethylamine 苯丙胺 Tyramine 色胺 octopamine 鱆鱼胺 Prostaglandin 前列腺素 catatonia 紧张症 Nitric oxide (NO) 一氧化氮
4. Questions 1) How many types of purinergic receptors? What is the action mode? 2) Why ATP is a neurotransmitter? 3) What is the mechanism of neurosteroid actions? Please illustrate by GABAA receptor. 4) How does NO biosynthesize in brain? What is the mechanism of NO in neuronal excitotoxicity? Disease of the Basal Ganglia:1. Requirement: 1) Understanding the concept of disease of the basal ganglia,the anatomy and functions of the basal ganglia,the function of direct and indirect pathways,the etiology of Parkinson’s disease,the principle the treatment for the Parkinson’s disease. 2) Possessing the knowledge of the anatomy and function of the nigrastrial pathway, neurotransmitters in the nigrastrial pathway,the causes of degeneration of dopamine neuron. 2. Contents: 1).Introduction 2).Anatomy of the basal ganglia The striatum:the caudate and the putamen The globus pallidus The substrantia nigra The subthalamic nucleus Neurotransmitters in the basal ganglia 3).The pathways: Direct pathway Indirect pathway 4).Parkinson’s disease Pathology of dopamine neuron in the substantia nigra Etiology of Parkinson’s disease The mechanism of movement diorder of Parkinson’s disease The principle for therapeutics of Parkinson’s disease 3. Key Words: The basal ganglia 基底神经节 Neurodegeneration 神经元退行性变 Parkinson’s disease 巴金森病 Nigrastrital pathways 黑质纹状体通路 4. Questions: 1) What are the components of the basal ganglia? 2) How are the structures of the basal ganglia connected? 3) Describe the corticostriatal projections. 4) Describe the connections between subthalamus and globus pallidus 5) Describe the importance of the nigrastrital pathways. 6) What is the role of the basal ganglia in relation tO the motor thalamus? 7) What are the principal neurotransmitters and receptors associated with the basal ganglia? 8) A disorder of the basal ganglia is indicated what signs? 9) Can administration of dopamine cure Parkinson’S disease?Why? 10) Describe the etiology Of neurodegeneration in the substantia nigra in PD 11) Why dose lesioning the SThn or GP reduce the symptoms of PD? Chapter 16 The Epilepsies1. Requirements: 10) Holding the definition, animal models, pathology of epilepsy; holding epilepsy-related neurotransmitters; holding approaches to the control of epileptic activity; holding antiepileptic drugs. 11) Knowing the classification of epilepsy; knowing the mechanism underlying epileptic animal models; knowing the mechanism underlying the action of antiepileptic drugs. 12) Understanding the development of an epileptic seizure. 2. Contents: 1) Definition of epilepsy 2) Classification of epilepsy 3) Animal models of epilepsy 4) Cause of pathology of epilepsy 5) Development of an epileptic seizure 6) Neurotransmitters in epileptic activity 7) Approaches to the control of epileptic activity 8) Antiepileptic drugs 3. Key words: epilepsy 癫痫 seizure 癫痫发作 Synchronous discharge 同步放电 Focus 癫痫灶 Temporal lobe epilepsy 颞叶癫痫 Partial seizure or epilepsy 部分性癫痫 Generalized seizures 全身性癫痫 Grand mal or tonic-clonic seizure 大发作或强直-阵挛发作 Petit mal or absence seizure 小发作或失神发作 Convulsion 惊厥 Myoclonic 肌阵挛 Electroencephalogram 脑电图 Spike wave 棘波 Electrical stimulation 电刺激 Chemical convulsants 化学致痫剂 Epileptogenesis 癫痫发生 Depolarization 去极化 Sprouting 出芽 Kainic acid 海人藻酸 Kindling 点燃 Hippocampus 海马 Amygdala 杏仁核 4. Questions: 1) What is epilepsy? 2) How are epileptic seizures classified? 3) Please give one or two samples for animal models of generalized seizures and partial seizures? 4) How is an epileptic seizure developed? 5) Please describe GABA function in epileptic activity. 6) Please list current approaches to control epileptic activity. 7) Please briefly explain possible mechanism of action of antiepileptic drugs, including old ones (phenytoin, carbamazepine, ethosuximide, barbiturates, benzodiazepines, valproic acid) and new ones (lamotrigine, vigabatrin, tiagabine, gabapentin). Chapter 17 Schizophrenia, Anxiety and Depression1. Requirements: 1) knowing symptoms of schizophrenia and aetiology of schizophrenia; therapy of schizophrenia; animal models of anxiety; drug treatments for anxiety; neurochemical basis of antidepressants 2) understanding the neurobiological basis of schizophrenia; the role of monoamines in anxiety; the role of central monoamine in depression 2. Contents: 1) Schizophrenia symptoms of schizophrenia; aetiology of schizophrenia; neurobiology of schizophrenia; therapy of schizophrenia 2) Anxiety animal models of anxiety; monoamines in anxiety; drug treatments for anxiety 3) Depression central monoamine and depression; neurochemistry of antidepressants 3. Key words: schizophrenia 精神分裂症 typical neuroleptics 典型抗精神病药 atypical neuroleptics 非典型抗精神病药 positive symptoms 阳性症状 negative symptoms 阴性症状 depression 抑郁症 affective disorders 情感性疾病 bipolar disorders 躁郁症 anxiety 抑郁症 4. Questions: 1) What is the neurobiological basis of schizophrenia? 2) How are monoamines involved in anxiety? 3) What are the roles of central monoamine in depression? 4) What are the common features of schizophrenia, anxiety and depression? Chapter18 Alzheimer Disease1. Requirements: 1) Knowing the the clinical symptoms, the prevalence and the etiology of Alzheimer’s disease (AzD); knowing the different types of senile plaques; knowing the relationship of neurotransmitters and memory, methods for testing memory function. 2) Holding what is dementia; holding that the failure of Ach system is related to the toxicity of b-amyloid; holding the relation between tau protein and neurofibrillary tangles. 3) Understanding the pathological changes of AzD; understanding the formation of b-amyloid and its effects; understanding the therapeutic strategy of AzD; understanding how to manipulate cholinergic system; relationship 2. Contents: 1) Introduction What is dementia? the causes of dementia; the clinical symptoms of Alzheimer’s disease (AzD); the prevalence of AzD; the pathological markers of AzD. 2) Pathology Senile plaques; neurofibrillary tangles; other pathological changes including neuronal loss, hirano bodies, cytoplasmic granulovacoular degeneration; formation of b-amyloid and its effects. 3) Etiology Genetic mutation; head injuries, aluminum, inflammation 4) Neurotransmitter changes in Alzheimer’s disease Acetylcholine (Ach); Ach and b-amyloid; monoamines; somatostatin, glutamate 5) Neurotransmitters in memory processing Memory and Long-term potentiation (LTP); acetylcholine and memory; glutamate and memory; other neurotransmitters. 6) Therapy Manipulation of neurotransmitters; attenuation of degeneration. 3. Key words: Alzheimer’s Disease
b-Amyloid
Amyloid precursor protein
Senile plaque
Tau protein
Neurofibrillary tangle
Paired helical filament
Apolipoprotein E (ApoE)
Presenilin
Degeneration
Cerebral cortex
Hippocampus
Frontal temporal cortex
The nucleus basalis
Secretase
Acetylcholine
Choline acetyltransferase (ChAT)
Acetylcholinesterase
Cholinesterase
Muscarinic receptors
Nocotinic receptors
Glutamate
Long term potentiation (LTP)
5-Hydroxytryptamine (5-HT)
Norepinephrine (NA)
4. Review Questions: 1.What are the pathological changes in AzD brain? 1. What are the pathological hallmarks of Alzheimer’s disease? 2. The pathological changes of Down Syndrome are similar to those of AzD. Do you think that there are same mechanisms in these two diseases? Why? 3. Is there a relationship between the toxicity of b-amyloid and clinical symptoms? Why? 4. Describe the changes of neurotransmitters in AzD brain. 5. Describe the potential therapeutic strategies for AzD. 6. Present evidences that the failure of Ach system is related to the toxicity of b-amyloid. 7. Explain main evidences that Ach is implicated in memory. 8. Describe the relationship between LTP and memory. 10. Describe the etiology of AzD. 第十五章 精神分裂症、焦虑症、抑郁症 教学内容 一精神分裂症 精神分裂症的症状;病因;病理机制;动物模型;治疗 二焦虑症 焦虑症的动物模型;焦虑症的发病机制;焦虑症的药物治疗 三抑郁症 抑郁症的神经生物学基础;抗抑郁药的作用机制
教学要求 了解精神分裂症的症状和病因;理解精神分裂症的病理机制;了解精神分裂症的动物模型和治疗;了解焦虑症的动物模型;理解焦虑症的发病机制;了解焦虑症的药物治疗;理解抑郁症的神经生物学基础;了解抗抑郁药的作用机制
专业英文词汇
schizophrenia 精神分裂症 typical neuroleptics 典型抗精神病药 atypical neuroleptics 非典型抗精神病药 positive symptoms 阳性症状 negative symptoms 阴性症状 depression 抑郁症 affective disorders 情感性疾病 bipolar disorders 躁郁症 anxiety 抑郁症 Pain and analgesia 1. Requirement: 1) Understanding the concept of nociceptor, the components and functions of the descending pathway and the ascending pathway in pain modulation,the formation of pain sensation. 2) Possessing the knowledge of the components of spinothalamic pathway, the Gate Theory, the function of the substantia gelatinosa in the transformation of nociceptive information,the neurotransmitters in the pain modulation,the function of opiates. 2. Contents: 1).Introduction 2).Peripheral events in the initiation of pain i).Sensory receptor-nociceptors ii).Tissue damage and chemical mediators 3).Central events in the transmission of pain i). Ascending pathway Sensory transmission in the spinal cord the spinothalamic pain pathway the trigemenal pathway ii). Central inhibitory system Descending pmhw~ Neurotransmission of descending pmhw~ PAG 4).Analgesia-opiates History of endogenous opiate Opiate receptors Analgesic mechanism 5).Neurotransmitters in pain formation Spinal cord Suraspinal cord 3. Key word: Nociceptor 伤害性感受器 Hyperalgesia 痛觉超敏 Substantia gelatinosa 罗氏胶质区 Analgesia 镇痛 Spinothalamic pathway 脊丘束 Periaqueductal gray matter (PAG) 中央灰质 Descending pathway 下行(抑制)通路 Ascending pathway 上行(激活)通路 4. Questions: 1) Describe which parts of peripheral tissue participate the transformation of nociception to the brain? 2) Describe the formation of pain. 3) Describe which parts of the central nervous system modulate pain sensation,and how? 4) Where within the body Can pain be modulated,and what causes its modulation? 5) Where in the central nervous system does information about pain converge? 6) Describe the deference between nociception and pain? 7) Where does substantia gelatinosa (SG)locate in the spinal cord? 8) Describe the main function of SG 9) What is the main function of the spinothalamic pathway? 10) What is the main function of the periaqueductal gray matter (PAG)?
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