2011年10月自考《生理心理学》必背知识3
生理心理学笔记总结归纳
精心整理第一章绪论1.生理心理学：生理心理学是研究心理现象的生理机制，即研究外界事物作用于脑而产生心理现象的物质过程的科学。
生理心理学正是以脑为中心，研究心理的生理机制或行为的生理机制。
2.研究对象和任务：生理心理学的研究对象是心理活动的生理机制，因此，研究并3.4.生理心理学研究方法和技术：●脑立体定位技术●脑损伤法●原理：大脑皮层机能定位说、大脑皮层机能等势说●具体方法：不可逆损伤:横断损伤吸出损伤电解损伤●可逆损伤:扩布性阻抑冰冻方法神经化学损伤●刺激法（电刺激法，化学刺激法）原理：任何心理和生理活动都是由神经系统的兴奋所引起，电刺激和化学刺激可以代替外部刺激。
●电记录法：原理：神经系统的兴奋是以生物电的形式表现出来的。
●生物化学分析法原理：机体活动受化学物质的影响（递质、受体），并且能●●耗竭能够提高皮层的脑电活动。
上行胆碱能系统的作用机制：一种可能性是胆碱能投射通过提高新意刺激的作用，帮助了刺激在皮层水平的加工，另一可能是通过提高信号/噪声比的机制而起作用。
4）上行5—HT系统的功能：5-HT的操作影响到与行为抑制有关的过程。
总结：蓝斑皮层NE系统有维持紧张或唤醒的情境下辨别能力的保护功能，因而参与了选择性注意的加工；中脑边缘DA系统和中脑纹状体DA系统有助于不同形式的行为激活，从而在认知或运动的传出中扮演重要角色；皮层胆碱能系统促进刺激在皮层水平的加工，在注意和记忆信息加工中处于基础地位；5-HT能系统有助于行为抑制即降低无关信息引起的活动，他与上述三个系统的功能是对立的。
这些上行网状模式，前额叶损伤导致了行动的选择性和组织性受到了破坏。
背外侧前额叶和扣带回是参与对许多不同新意刺激或微弱提示活动的注意的脑区。
注意的生理学过程：注意的转移机制：优势兴奋中枢的转移——优势兴奋中心从其他区域转移到这种强烈刺激的皮层代表点。
注意产生的中枢过程是兴奋和抑制的相互诱导大脑皮层上兴奋和抑制的相互诱导服从于优势原则——当有集体把某种事物作为自己心理活动的对象时，该事物在大脑皮层上引起一个强烈的优势兴奋中心，这个优势兴奋中心对皮层其他区域较弱的兴奋起抑制作用。
生理心理学复习重点
生理心理学复习重点1、静息膜电位：在静息状态下，由于细胞膜内外离子浓度的不同，存在着电位差，这种电位差就称为……或在静息状态下，细胞膜外钠离子浓度较高，细胞膜内钾离子浓度较高，这类带电离子因膜内外的浓度差造成了膜内外大约负70-90毫伏的电位差，称之为静息电位（极化现象）。
2、神经冲动的传导：全或无定律、级量反应All-or-none law：每个神经元都有一个刺激阈值，对阈值以下的刺激不发生反应，即“无”反应；而对阈值以上的刺激，不论其强弱均给出同样高度（幅值）的神经脉冲发放，即“全”反应。
（该定律只适用于单根神经纤维中，只说明兴奋的传导过程，而不是产生过程）级量反应：在神经冲动的产生过程中，首先引起一个局部反应，而局部反应的大小与刺激的大小有关，只有当总和的兴奋性突触后电位累加超过了阈值，就会产生一个脉冲。
3、突触类型：轴-轴、轴-胞体、轴-树4、突触传递的特点：（1）单项传递：前膜——〉后膜（2）突触延搁：从感应器接收到刺激到效应器开始出现反射活动所经历的时间。
（3）易化作用：部分去极化后对下一次冲动更容易引起反应。
（4）抑制：前膜释放的递质并不能使后膜产生兴奋，反而是抑制。
（5）总和：微弱刺激反复作用，使后一神经元阈下兴奋产生叠加，足以使其产生神经冲动。
（6）疲劳：当递质的消耗比释放更快的时候，突出产生疲劳。
（7）药物的作用：特异性的阻断或促进突触传递。
5、EPSP：若突触前神经元所释放的神经传递物质与突触后神经元的接受器结合后，会引起突触后神经元去极化的反应，使更容易达到阈值而产生动作电位，称为兴奋性突触后电位。
IPSP：若突触前神经元所释放的神经传递物质与突触后神经元的接受器结合后，会引起突触后神经元过极化的反应，使更难达到阈值而产生动作电位，称为抑制性突触后电位。
6、神经递质：凡是神经细胞间神经信息传递中介的化学物质，统称神经递质。
7、受体：受体是细胞膜上的特殊蛋白分子，可以识别和选择性地与某些物质发生特异性受体结合反应，产生相应的生物效应。
生理心理学
1.生理心理学是通过实验的方法研究外界事物作用于脑而产生心理现象的生理过程，主要揭示人类自身心理现象和行为的生理机制的科学。
心理学+信息科学+神经科学2.生理心理学研究技术和方法：脑立体定位技术、脑损伤法、刺激法、电记录法、生物化学分析法、分子遗传学法、脑成像技术。
3.电刺激法：用无伤害性的电流刺激脑的特定部位，观察心理行为的变化以确定该脑部位的功能；或者在使用电流刺激脑的某部位时记录其他脑部位的诱发电位等，以推测两个或多个脑区之间是否存在直接或间接关系。
4.化学刺激法：在脑的局部区域注射神经递质的激动剂等，观察它们对心理行为的影响。
警觉网络--影响注意系统从而改善对目标的动作速度脑内网状上行激活系统（去甲肾上腺素、多巴胺、胆碱、5-羟色胺）5.注意的神经网络定向网络--调整注意焦点到目标区域，并限制对指向区域的信息的输入。
顶叶、中脑的上丘和丘脑执行网络--注意的目标选择并执行。
额叶的部分区域包括扣带回6.注意从其产生的方式上来说是一种定向反射；注意产生的中枢过程是兴奋和抑制的相互诱导。
敏感化：神经系统中一些特殊细胞对任何刺激都有反应，随着刺激强度增大，更多的细胞参与反应，若某较弱刺激持续作用，相应的神经元放电也7.神经活动过程的双重模型会增加。
习惯化：某刺激重复出现时，参与相应反应的神经细胞就会疲劳；随刺激的每次重复，细胞的反应逐渐减弱。
8.感受器的适宜刺激：某能量形式的刺激作用于感受器，只需要极小强度就能引起相应的感觉。
这种能量刺激形式或种类就是该感受器的适宜刺激。
9.换能作用：感受器把作用于他们的各种有效刺激转换为相应的传入神经纤维上的动作电位或峰电位。
10.动作电位：是指可兴奋细胞受到刺激时在静息电位的基础上产生的可扩布的电位变化过程。
11.感受器的适应现象：刺激作用于感受器时，刺激仍在持续作用，但神经纤维的传入冲动频率已开始下降。
12.三级细胞：光感受细胞（视杆+视锥）；双极细胞；神经节细胞13.外侧膝状体：给光中心和撤光中心通道；XYW通道；左右信息通道；方位敏感性信息通道；空间频率通道；运动方向信息通道；颜色信息通道14.视皮层功能柱：有相同功能特性的皮层细胞，按规则的空间结构排列起来构成柱状。
自考《生理心理学》必背知识
情绪与情感的生理心理学帕帕兹认为在边缘系统结构中，从海马经穹窿、乳头体、丘脑前核和扣带回，再回到海马的环路（帕帕兹环路），对情绪产生具有重要作用。
情绪的激活学说和情绪的边缘系统学说集中地表达了现代神经生理学关于脑高级功能的理论成果。
把网状结构和边缘系统的功能特点与情绪和情感过程联系起来，与巴甫洛夫以前经典神经生理学对于情绪的理论相比，不但具有整体和器官水平的实验证据，还有细胞生理学的实验依据。
还有许多著名的经典实验，对情绪生理心理学的发展具有重要历史意义，如假怒实验、怒叫反应和自我刺激实验等。
◎什么是假怒，切除猫的大脑皮层之后，猫对各种不愉快的刺激如轻触、气流等均表现出极度夸大的攻击性行为表现：弓腰、竖毛、咆哮、嘶叫和张牙舞爪等。
这些行为缺乏指向性，很难说动物伴有怒的内心体验，所以将这种动物的行为表现称作“假怒”。
实验证明只要手术破坏边缘皮层、大脑皮层与下丘脑的神经联系，使大脑皮层对下丘脑的抑制解除，下丘脑机能亢进就会出现“假怒”。
△□我国生理学家卢于道和朱鹤年于 1937 年电刺激脑中枢，发现猫能发出呻吟的声音。
1952 年他们又深入研究了猫中脑的怒叫中枢。
△□下丘脑、隔区、杏仁核、海马、边缘皮层、前额皮层和颞叶皮层等均是情绪过程的重要脑中枢。
边缘系统在体内环境平衡和情绪活动中，具有重要作用。
◎皮肤电反应是由皮肤电阻或电导的变化而造成的。
皮肤电阻或电导随皮肤汗腺机能变化而改变。
交感神经兴奋，汗腺活动加强，分泌汗液较多。
由于汗内盐成分较多使皮肤导电能力增高，形成大的皮肤电反应。
皮肤电反应只能作为交感神经系统功能的直接指标，也可以作为脑唤醒、警觉水平的间接指标，但无法辨明情绪反应的性质和内容。
第十章运动和意志行为◎每个脊髓运动神经元及其所支配的骨骼肌纤维称为运动单位。
平滑肌、腺体和心肌接受植物性神经支配。
植物性神经末梢和它们之间的接点统称为神经效应器接点。
△肌梭是一种特殊的本体感受器，即肌肉长度变化的感受器。
自学考试《生理心理学》复习要点总结
裂脑手术：为治疗一种癫痫偶尔进行的脑手术，医生切开连接大脑两半球的胼胝体。
切开胼胝体的病人就是裂脑人。
2．杏仁核：颞叶嘴端内部的结构，包括一系列的核，是边缘系统的组成部分。
恐惧中枢——杏仁核实验证据：杏仁核毁损可阻断大鼠对天敌和新异事物的恐惧。
刺激杏仁核可引起类似恐惧样的行为表现条件化学习和记忆中枢——杏仁基底外侧核条件恐惧表达中枢——杏仁中央核海马：海马：学习和记忆的重要脑区双侧海马受损会导致空间记忆严重破坏海马损伤导致的顺行性遗忘症3. 精神药理学：研究药物对神经系统和行为的效应科学。
拮抗剂：能对抗和抑制特定神经递质的突触后效应的药物。
安慰剂：给予有机体的一种替代生理活性药物的无活性物质，可用于控制实验中的给药效应。
4. 实验毁损法：实验动物脑组织的部分移除或毁损；可以推测，动物丧失的功能即是被毁损脑区的功能。
脑毁损研究是实验毁损法的同义词。
5. 光感受器：三原色编码我们的眼睛有三种不同的感受器，分别对三种不同的色调敏感。
人们能够看到的任何一种颜色，都可以通过混合光谱上的三种颜色获得。
三种视锥细胞：红，绿，蓝。
色觉就是由这三种视锥细胞负责的三种色觉缺陷：（1）红色盲：患者不能分辨红色和绿色，他们的视敏度是正常的，说明视网膜上不缺乏红绿视锥。
他们的红视锥细胞中填充的是绿视锥细胞的视蛋白。
（2）绿色盲，也不能分辨红色和绿色。
他们的绿视锥里填充的是红视锥细胞的视蛋白。
（3）蓝色盲，他们的视网膜上缺乏蓝视锥，视敏度没有受到明显的影响。
视网膜节细胞：对立加工编码红色和绿色为一对，黄色和蓝色为一对。
于是，视网膜上有两种颜色敏感性节细胞：红-绿细胞与黄-蓝细胞。
部分颜色敏感节细胞以中心-外周的方式进行反应。
对颜色不敏感的节细胞也接收视锥细胞的传入信息，但不同波长的光对于它们来说没有差别，它们只是简单地在其感受野的中心部和外周部编码视觉信息的相对亮度，这些细胞的作用相当于“黑-白-探测器”。
视网膜节细胞对不同波长的光的反应特征取决于三种视锥细胞与两种节细胞之间的神经回路的特点。
2011年10月自考《生理心理学》必背知识汇总
2011年10月自考《生理心理学》必背知识汇总1987年以来，逐渐将受体按其发生的生物效应机制和作用加以分类，如G-蛋白依存性受体家族、电压门控受体和自感受体等。
神经细胞间信息传递的化学机制并非总是如此复杂，当那些电压门控受体与神经递质结合时，就会直接导致突触后膜的去极化，产生突触后电位。
脑重量约占全身体重的2%，但其耗氧量与耗能量却占全身的20%，而且99%利用葡萄糖为能源代谢底物，又不像肝脏、肌肉等其他组织那样，本身不具糖元贮备，主要靠血液供应葡萄糖。
第一章感觉特异感觉系统和非特异感觉系统感受阈值：即刚能引起主观感觉或细胞电活动变化的最小刺激强度。
感受器的适应：随着刺激物长时间持续作用，感受灵敏率下降，感受阈值增高，此现象称感受器的适应。
感受野：把有效地影响某一感觉细胞兴奋性的外周部位，称为该神经元的感受野。
如果把微电极插在视觉中枢的某个神经元上，记录其电活动，凡能引起其电活动显著变化的视野范围，就是该视觉神经元的感受野。
第一节视觉眼的基本功能就是将外部世界千变万化的视觉刺激转换为视觉信息，这种基本功能的实现，依靠两种生理机制，即眼的折光成像机制和光感受机制。
前者将外部刺激清晰地投射到视网膜上，后者激发视网膜上化学和光生物物理学反应，实现能量转化的光感受功能，产生是感觉信息。
眼动的生理心理学机制：通过眼外肌肉的反身活动，保证使运动着的物体或复杂物体在网膜上连续成像的机制，也就是眼动的生理心理学机制。
眼睛的随意运动有哪几种方式?它的生理心理学意义是什么?答：眼睛的运动有许多方式，当我们观察位于视野一侧的景物又不允许头动时，两眼共同转向一侧。
两眼视轴发生同方向性运动，称为共轭运动。
正前方的物体从远处移向眼前时，为使其在视网膜上成像，两眼视轴均向鼻侧靠近，称为辐合。
物体由眼前近处移向远处时，双眼视轴均向两颞侧分开，称为分散。
辐合与分散的共同特点是两眼视轴总是反方向运动，称为辐辏运动★。
辐辏运动和共轭运动都是眼睛的随意运动。
2011年10月自考《生理心理学》必背知识4
SAGE-Hindawi Access to ResearchCardiology Research and PracticeVolume2011,Article ID532620,6pagesdoi:10.4061/2011/532620Research ArticleEffect of Exercise Training on Interleukin-6,Tumour Necrosis Factor Alpha and Functional Capacity in Heart Failure Neil A.Smart,1,2Alf rsen,3,4John P.Le Maitre,5and Almir S.Ferraz61Faculty of Health Science,Bond University,QLD4229,Australia2Department of Exericse Physiology,University of New England,Armidale NSW2351,Australia3Department of Cardiology,Stavanger University Hospital,4068Stavanger,Norway4University of Bergen,Institute of Medicine,5020Bergen,Norway5Mazankowski Alberta Heart Institute,Edmonton,Alberta,Canada T6G2B76Cardiovascular Rehabilitation Section,Institute Dante Pazzanese of Cardiology,S˜a o Paulo04011-002,BrazilCorrespondence should be addressed to Neil A.Smart,n smart@Received5October2010;Revised12January2011;Accepted14January2011Academic Editor:Gregory GiamouzisCopyright©2011Neil A.Smart et al.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use,distribution,and reproduction in any medium,provided the original work is properly cited.Background.We pooled data from four studies,to establish whether exercise training programs were able to modulate systemic cytokine levels of tumour necrosis factor-alpha(TNF-alpha)and interleukin-6(IL-6).A second aim was to establish if differences in ExT regimens are related to degree of change in cytokines and peak VO2.Methods.Data from four centres relating to training protocol,exercise capacity,and cytokine measures(TNF-alpha and IL-6)were pooled for analysis.Results.Data for106CHF patients were collated(98men,age62±10yrs,wt79±14Kg).Patients were moderately impaired(peak VO216.9±4.4mls/kg/min),with moderate LV systolic dysfunction(EF30±6.9%),78%(83)had ischaemic cardiomyopathy.AfterExT,peak VO2increased1.4±3.4ml/kg/min(P<.001),serum TNF-alpha decreased1.9±8.6pg/ml(P=.02)and IL-6was not significantly changed(0.5±5.4pg/ml,P=.32)for the whole group.Baseline and post-training peak VO2changes were not correlated with change in cytokine levels.Conclusions.Exercise training reduces levels TNF-alpha but not IL-6in CHF.However, across a heterogenic patient group,change in peak VO2was not correlated with alterations in cytokine levels.While greater exercise volume(hours)was superior in improving peak VO2,no particular characteristic of ExT regimes appeared superior in effecting change in serum cytokines.1.IntroductionInflammatory activation with increased serum cytokine levels has been described by several authors as an important factor in the progression of the syndrome of chronic heart failure(CHF)[1–3].In multifactorial analyses,elevated lev-els of tumour necrosis factor-(TNF-)alpha and interleukin-(IL-)6have been identified as prognostic heart failure markers[4–6].Cytokines act as catabolic factors involved in the pathogenesis of muscle wasting and cardiac cachexia [3,7],and increased levels of serum TNF-alpha have been identified in patients with reduced skeletal muscle cross-sectional area and peripheral muscle strength[1].There also exists a statistical significant association between elevated serum cytokine levels(especially TNF-alpha)and New York Heart Association(NYHA)functional class as well as exercise intolerance[2].Inflammatory cytokines may alter skeletal muscle histology and have a negative impact on left ventricular remodelling and cardiac contractility[2, 3,8].The inflammatory response is also associated with progression of atherosclerosis[9],oxidative stress[10],NO impairment[11],vasoconstriction,endothelial cell apoptosis [12],and adverse vascular remodelling[13].Exercise training has been documented to improve the inflammatory profile in CHF by inhibition of cytokine-chemokine production,regulation of monocyte activation and adhesion,inhibition of inflammatory cell-growth signals and growth factor production,reduction of soluble apoptosis signalling molecules[12],and attenuation of monocyte-endothelial cell adhesive interaction[14].A study of277 patients with coronary artery disease reported a significant 41%reduction in high-sensitivity C-reactive protein following exercise training[15].A recent study of four-month duration,utilizing combined endurance/resistanceTable1:Studies identified in PUBMED,MEDLINE search.Study Subjects(Control)Year Cytokines measured% VO2Mode of Exercise Adamapoulos et al.[23]122001Soluble adhesion molecules13Home bike Adamopoulos et al.[12]242002TNF-alpha,Interleukin-615Home bikeConraads et al.[16]23(12)2002TNF-alpha,Interleukin-67.5Bike and resistance training Ferraz et al.[21]#30(10)2004TNF-alpha,Interleukin-623BikeGielen et al.[2]20(10)2003TNF-alpha,Interleukin-1,6andbetaIn both serum and skeletal muscle29BikeKaravidas et al.[24]16(8)2006TNF-alpha,Interleukin-6,107.5∗Electrical stimulationLarsen et al.[22]#282001TNF-alpha,Interleukin-6,88∗Aerobic endurance training and home bikeLarsen et al.[25]252008Plasma Chromogranin A(CgA)8∗Aerobic endurance training and home bikeLaoutaris et al.[26]382007TNF-alpha,Interleukin-612Low versus high intensity inspiratory muscle trainingLeMaitre et al.[17]#462004TNF-alpha,Interleukin-63Bike and electricalstimulationNiebauer et al.[27]18(9)2005TNF-alpha Interleukin-6,e-selectin11BikeSmart[28]#222008TNF-alpha,Interleukin-6,brainnatriurietic peptide(BNP)20BikeXu et al.[18]60(28)2002TNF-alpha Unknown Unknown ∗%change in6-minute walk distance(Peak VO2not measured).#Study used in this paper.training demonstrated reduced TNF-alpha receptor levels (TNFR1and TNFR2)and a significant(7.5%)increase in peak VO2in patients with ischemic cardiomyopathy, although changes in IL-6and TNF-alpha were not apparent [16].This effect on circulating levels of TNF-alpha receptors is also reported after6weeks of cycle ergometry[17].In this study,there were no alterations in IL-6,C-reactive protein (CRP),or TNF-alpha.In addition,electrical muscle stim-ulation provided no changes in any of the aforementioned rsen et al.[8]reported an11%increase in peak VO2following3months of endurance training;TNF-alpha was significantly reduced,and this decrease was significantly correlated to the increase in peak VO2.Adamopoulos[14] reported a13%increase in functional capacity with a 12-week cycle ergometry training program,which correlated with lower levels of soluble adhesion molecules.The authors later reported a strong and highly significant correlation between improvements in peak VO2(15%)and reduction in TNF-alpha,soluble TNFR-1and-2,and IL-6[12].Plasma TNF-alpha is also documented to decrease after twice daily6-minute walk tests in NYHA II/III heart failure patients[18].A recently published study reported absent von Willebrand factor(vWF)release upon exercise testing in heart failure patients;this normalised following6months of exercise training;other plasma endothelial markers were unaltered [19].Changes in skeletal muscle,but not systemic expression of TNF-alpha,IL-1-beta,and IL-6have been reported in heart failure patients undertaking a regimen of10minutes cycling,4–6times daily for6months[2].This exercise program resulted in large changes in functional capacity (29%),nearly twice the mean expected increment(17%) shown from our review of81heart failure exercise training studies[20].This study suggested the existence of a cytokine cascade where levels may be changed at altered rates in different tissues.As heart failure exercise training studies are often small,we sought by pooling data from four studies to establish whether exercise training programs were able to modulate systemic cytokine levels.A second aim was to establish if differences in ExT regimens are related to the degree of change in cytokines and peak VO2.2.MethodsWe searched PUBMED and MEDLINE for exercise training studies in heart failure patients that had measured one or more of the proinflammatory cytokines.The full list of studies is summarized in Table1.The focus of this work was interleukin-6and TNF-alpha as these cytokines were measured in10exercise training studies,the correspondence authors of which were contacted for their cooperation in collaboration.Authors were requested to provide individual patient data from their study;four centres provided data (Table2).One study was a conference proceedings abstract [21].Sufficient data were not available to analyse changes in other cytokines.Table2:Clinical characteristics and pharmacotherapy of the106 patients.Clinical characteristicsAge(Years)61.8±9.9 Male(%)98(92.5) Body mass(kg)78.7±13.7 Peak VO2(ml·kg−1·min−1)16.9±4.4 Diabetes(%)11(10) Previous myocardial infarction(%)86(81) Atrialfibrillation(%)27(26) NYHA class II/III49/57 LVEF(%)30±6.9 MedicationsBeta-blocker(%)44(42) ACE-inhibitor/antagonist(%)95(90) Digoxin(%)67(63) Nitrates(%)40(38)2.1.Blood Sampling and Analysis.In3studies,plasma or serum samples were obtained by venipuncture(arterial cannula used in Larsen’s study)and stored on ice.In all studies,venipuncture collections were taken between 0900,and1200,at least24hours and not more than 5days after the last exercise session,thus negating the effects of the intervention.Within one hour,samples were centrifuged at4◦C,1500–2000RPM for10minutes,and then separated into aliquots and stored at between−75◦C and −80◦C.Concentrations of IL-6or TNF-alpha were measured by commercially available enzyme-linked immunosorbent assays(ELISAs)(R&D systems Minneapolis,Minnesota) in all4studies.The intra-and interassay coefficients ofvariation were<10%for all assays.In one study,16healthy, male volunteers of approximately the same age(62±5years) served as controls[22]although this data was not included in our analyses.2.2.Metabolic Exercise Testing and Exercise Training.All four collaborating investigators completed baseline and posttraining metabolic exercise tests to establish functional capacity.Larsen and Smart used cycle ergometers with a15W and 10W per min stepped protocol,respectively;LeMaitre and Ferraz used a modified Bruce treadmill protocol.One study used a regime of supervised aerobic exercise training3times per week.Two studies used supervised cycle ergometry as the primary mode of exercise training[21,22], and one study used both home-based and neuromuscular stimulation of the legs[17].2.3.Data Extraction.Mode of training,program duration and exercise intensity were examined.Baseline and post-training cytokine levels,peak VO2,left ventricular ejection fraction(LVEF),clinical,demographic,and pharmacological characteristics of patients are shown in Table2.Table3:Exercise program parameters and change in primary outcome measures in the4studies.Ferraz Larsen LeMaitre Smart Weeks2412616 Minutes/Wk1359015090 Freq.sessions/Wk3353 Intensity(%max)67807070 Total hours545415482.4.Statistical Analysis.Paired student t-tests were used to analyse baseline and postintervention changes in cytokines and peak VO2.ANOV A(2×4)was used to analyse differences between the four datasets.Pearson correlation coefficients were established for change in cytokines and peak VO2.Univariate and multivariate regression analysis with change in TNF-alpha as the dependent variable were used to determine factors leading to cytokine change.Data are expressed as mean+/−standard deviation unless otherwise stated.Significance was accepted at the5%level(P<.05).3.Results3.1.Baseline Measures.The four collaborating authors pro-vided data on106patients(98male,age62±10yrs,body weight79±14Kg).Patients were moderately impaired(peak VO216.9±4.4mls/kg/min),with moderate LV systolic dys-function(EF30±6.9%).Seventy eight%(83)had an ischaemic cardiomyopathy(Table2).Adherence data relating to training regimes were87.2±1.9%[21]and85±12%[28] and were unavailable for the other2studies.3.2.Training Regimes.Regimes varied between3and5 exercise sessions per week,at an intensity of58–80%of peak VO2.Program durations were between6and24weeks, 90–150minutes per week,and total program hours varied between15and54hours(Table3).3.3.Pooled Posttraining Changes.After training,peak VO2 increased by1.4±3.4mL/kg/min or9%(P<.001)from 16.9±4.4to18.4±4.5,serum TNF-alpha decreased from a baseline value of13±15.2pg/mL by1.9±8.6pg/mL(P= .02),and IL-6increased slightly from a baseline value of 7.8±11.4pg/mL by0.5±5.4pg/mL(P=.32).Cytokinechanges for each study can be seen in Figure1.Body weight was unchanged following exercise training.None of the clinical,demographic,or pharmacologic variables were correlated with changes in circulating IL-6or TNF-alpha following training.The correlations between change in posttraining peak VO2and changes in TNF-alpha(r=0.023, P=.82)and IL-6(r=−0.12,P=.21)were not significant. Change in TNF-alpha was correlated with exercise session duration and anerobic threshold(both r=0.21,P= .31),univariate but not multivariate analysis identified that previous myocardial infarction,longer exercise session duration,and higher body mass index predicted change in TNF-alpha(r2=0.18,P=.001).302520151050−5−10−15−20−25IL-6TNF-αPeak VO 2Figure 1:Change in cytokines and peak VO 2across the four studies.3.4.Optimal Exercise Program Components for Peak VO 2and Cytokine Changes.A total exercise program duration of 54hours appeared to be superior than 15or 18hours in e ffecting change in peak VO 2(P <.001);however,no di fference was seen for change in cytokine levels.The longest program duration resulted in a greater increment in peak VO 2compared to 12weeks (P =.003)and 6weeks (P =.001),while peak VO 2or 6-minute walk distance was unchanged in the ExT programs of 6and 12weeks duration.4.DiscussionPooled data from four studies demonstrated that alterations in levels of the cytokines IL-6and TNF-alpha are not nec-essarily uniform.Increments in peak VO 2following exercise training are widely accepted;however,they may be unrelated to changes in cytokine levels.Moreover,changes in particular cytokines appear to be independent of one another.One can-not be sure about the variable e ffects of the di fferent program parameters and exercise adherence rates;nevertheless,the mean change in functional capacity from the four studies was 8%,suggesting that cumulatively the four exercise programs provided stimulus for a possible favourable change in cytokine expression.Interpretation of this pooled data is limited by the fact that several other centres did not supply data.Table 2suggests that study participants showed heterogeneity for age,peak,VO 2and beta-blocker use.4.1.Expectations of Favourable Changes in Cytokine Expres-sion.Moderate endurance activity in frail,elderly,but otherwise healthy persons has previously been reported to influence circulating cytokine levels [29].As our patients had mild to moderate heart failure,it is not surprising to observe that levels of systemic TNF-alpha were decreased after training,thereby initiating anti-inflammatory e ffects.The finding that IL-6was unchanged after training is more puzzling.However,one study has suggested that IL-6produced by exercising muscle is thought to exert an anti-inflammatory e ffect [30].These data suggest that production and removal of TNF-alpha and IL-6may be,at least partially,from independent mechanisms and may have opposing e ffects (inflammatory versus anti-inflammatory).Recent clinical trials have not shown benefit from treatments that target TNF-alpha.A clinical trial of etanercept (a TNF-alpha antagonist)therapy has cast doubt on the role of cytokines in the pathogenesis of heart failure [31].There are then implications for health professionals or researchers in the process of designing an exercise program for heart failure patients.Primary end points of CHF exercise programs should perhaps not include lowering cytokine levels as they may represent surrogate markers of e fficacy;this may be particularly true in patients with milder degrees of CHF.In this population,program design may be better focussed on the parameters such as program frequency (sessions/week),duration (number of weeks),and intensity that may have a greater e ffect on peak VO 2changes.Peak VO 2improvement from exercise training may be linked to attenuated levels of oxidative stress which in turn may attenuate cytokine expression.Previous work in healthy older adults [32]and heart failure patients [33]has shown intermittent exercise programs to be at least more e ffective in improving peak VO 2than a continuous regime that would produce greater cumulative oxidative stress.In our work,peak VO 2was not significantly changed in patients who exercised despite utilizing a reasonable volume of exercise to elicit functional capacity changes.In heart failure,the e ffect of inflammation,which may be due partly to inactivity,may manifest in the terminal disease phase.The study by Adamopoulos et al.[14]may provide the best evidence to date linking change in peak VO 2and cytokines in heart failure patients.The small cytokine change shown in our studies may be due to the fact that our patients exhibited mild to moderate heart failure symptoms.The par-ticipants in the study of Adamopoulos et al.[14]exhibited moderate to severe symptoms.In addition,our participants had higher left ventricular ejection fractions (30%versus 24%)than those of Adamopoulos et al.[14].Exercise train-ing has been shown to significantly reduce the local muscle expression of TNF-alpha,IL-1-beta,IL-6,and iNOS in the skeletal muscle of CHF patients [8].In turn,physical exercise has been shown to improve both basal endothelial nitric oxide (NO)formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF.The correction of endothelium dysfunction is associated with a significant increase in exercise capacity [34].These local anti-inflammatory and systemic e ffects of exercise may attenuate the catabolic wasting process associated with CHF progression [3].In addition to an overall beneficial e ffect on exercise capacity,combined endurance/resistance exercise training has an anti-inflammatory e ffect in patients with heart disease [16].These skeletal muscle and anti-inflammatory changes may explain why alterations in TNF-alpha levels are most likely to be observed in patients with moderate or severe heart failure.4.2.Conclusions.Exercise training reduces levels of TNF-alpha but not IL-6in CHF.However,across a heterogenic patient group,change in peak VO2was not correlated with alterations in cytokine levels.While greater exercise volume (number of hours)was superior in improving peak VO2,no particular characteristic of ExT regimes appeared superior in effecting change in serum cytokines. 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生理心理学必备考点
生理心理学必备考点生理心理学期末复习1. “全或无”定律每个神经元都有一个刺激阈值，对阈值以下的刺激不发生反应，对阈值以上的刺激，不论其强弱均给出同样幅值的神经脉冲发放。
2. 统觉性失认症患者对一个复杂事物只能认知其个别属性,但不能同时认知事物的全部属性,故又称同时性视觉失认症。
这种失认症可能是V2区皮层以及与支配眼动的皮层结构间联系受损,如与中脑的四叠体上丘或顶盖前区眼动中枢的联系遭到破坏,不能通过眼动机制连续获得外界复杂物体的多种信息3. 感受野在神经系统中，每一个神经元在它的感受器都有其代表区（范围），只要这个代表区受到刺激，这个神经元就产生反应，这个代表区就被称为神经元的感受野。
4. 功能柱具有相同感受野并具有相同功能的视皮层神经元，在垂直于皮层表面的方向上呈柱状分布，只对某一视觉特征发生反应，从而形成了该种视觉特征的基本功能单位。
5. 朝向反射由新异性强刺激引起机体的一种反射活动，表现为机体现行活动的突然中止，头面部甚至整个机体转向新异刺激发出的方向，通过眼耳的感知过程探究新异刺激的性质及其对机体的意义。
6. 多模式感知细胞颞下回的一些神级元，不仅对复杂视觉刺激物单位发放率增加和发生最大的反应，而且对多种其他感觉刺激均可引起其单位发放率的变化。
因此，这类神级元称为多模式感知细胞。
7. ADHD儿童注意缺陷多动障碍8.失认证是感觉到的物象与记忆的材料失去联络而变得不认识。
9.辐辏运动正前方的物体从远处移向眼前时，为使其在视网膜上成像，两眼视轴均向鼻侧靠近，称为辐合；相反，物体由眼前近处移向远处时，双眼视轴均向两颞侧分开，称为分散。
辐合与分散的共同特点是两眼视轴总是反方向运动，称为辐辏运动。
10. 中枢神经系统中枢神经系统分为脊髓和脑，脑又分为大脑小脑间脑脑干，脑干又包括延脑桥脑中脑。
11. 级量反应其电位的幅值随阈上刺激强度增大而变高，反应频率并不发生变化。
简答题1.简述感觉系统的基本功能①区别不同形式的能量②反应刺激的不同强度和质量③反应的信度④反应的速度⑤抑制无关信息2. 知觉的恒常性是指什么？当客观事物本身不变，但它给予我们的感觉刺激，由于某些别的条件的变化而在一定限度内有变化时，我们的知觉不变。
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第三章知觉的生理心理学
一、知觉的神经基础
①在各种感觉功能的大脑皮层中，存在着两级功能区，即初级感觉区和次级感觉区。
②在各种性质不同的皮层感觉区之间还存在着联络区皮层。
③次级感觉皮层、联络区皮层以及与记忆功能有关的脑结构，形成了知觉的神经基础。
失认症及说明的问题?失认症是一类神经心理障碍，患者意识清晰，注意力适度，感觉系统与简单感受功能正常无恙，但却不能通过该感觉系统识别或再认物体，对该物体不能形成正常知觉。
失认症患者的一级感觉皮层功能完全正常，但次级感觉皮层或联络区皮层存在着局部的器质性损伤。
根据脑损伤的部位和程度，可出现不同类型的失认症：包括视觉失认症、听觉失认症和躯体失认症。
1.视觉失认症的类型：统觉失认症、联想失认症、颜色失认症、面孔失认症。
患者的初级视皮层17区、外侧膝状体、视觉通路、视神经和眼的功能和结构均正常无损;脑局部损伤可分为在2—4视觉皮层区(V2，V3，V4)或颞下回、颞中回、颞上沟，也常见枕-颞间的联络纤维受损。
①统觉性失认症：患者对一个复杂事物只能认知其个别属性，但不能同时认知事物的全部属性，故又称同时性视觉失认症。
这种失认症可能是V2区皮层以及与支配眼动的皮层结构间联系受损，如与中脑的四叠体上丘或顶盖前区眼动中枢的联系遭到破坏，不能通过眼动机制连续获得外界复杂物体的多种信息。
②联想性失认症：患者能对物体的各种属性分别得到感觉信息，并进行综合认知，很好完成匹配任务，正确描述物体的形状、颜色等属性;但患者却不知物体的意义、用途，无法称呼物体的名称。
这类患者大多数是由于颞下回或枕-颞间联系受损而致。
这是视觉及其记忆功能和语言功能之间的功能解体所造成的。
③面孔失认症：分熟人面孔失认症和陌生人面孔分辨障碍。
熟人面孔失认症对站在面前的两个陌生人可知觉或分辨，也能根据单人面孔照片，指出该人在集体照片中的位置。
但病人不能单凭面孔确认亲人，却可凭借亲人的语声或熟悉的衣着加以确认。
这类病人大多数是双侧
或右内侧枕-颞叶皮层之间的联系受损。
陌生人面孔分辨障碍的患者，对熟人确认正确无误，但对面前的陌生人却无法分辨。
这类患者大多数为两侧枕叶或右侧顶叶皮层受损。
2.听觉失认症：患者大脑初级听皮层(颞横回的41区)、内侧膝状体、听觉通路、听神经和耳的结构与功能无异常所见，但却不能根据语音形成语词知觉或不能分辨乐音的音调，也有患者不能区别说话人的嗓音。
词聋患者大多数左颞叶22区或42区次级听觉皮层受损所致。
乐音失认症患者，多为右颞22区、42区次级听皮层受损所致。
3.体觉失认症：顶叶皮层的中央后回(3-1-2区)躯体感觉区结构与功能基本正常，但此区与记忆功能和语言功能的脑结构间联系受损，引起皮层性触觉失认症，实体觉失认症等多种类型的体觉失认症。
实体觉失认症，多为右半球顶叶感觉区与记忆中枢间的联系障碍，引起左手触觉失认症状。
总结：从上述多种类型的失认症中得出结论——失认症是知觉障碍，不是因该感觉系统的损伤，而是由高层次脑中枢间的联络障碍所致。
证明知觉是许多脑结构和多种脑中枢共同活动的结果。
即使是以其中一种感觉系统为主的知觉，无论是视知觉、听知觉还是躯体知觉，也是这些感觉系统与注意、记忆、语言中枢共同活动的产物。
二、知觉的细胞生理学基础
1.视觉功能柱、超柱及超柱的特征提取(多模式感知细胞及生理意义)
(1)功能柱：具有相同感受野并具有相同功能的视皮层神经元，在垂直于皮层表面的方向上呈柱状分布，只对某一种视觉特征发生反应，从而形成了该种视觉特征的基本功能单位，所以称之为功能柱。
功能柱是感觉的基础。
有两种功能柱理论：特征提取功能柱和空间频率功能柱。
(2)超柱：在大脑视觉皮层中，具有相同感受野的多种特征检测细胞聚集在一起，形成了对各种视觉属性综合反应的基本单元，就是超柱。
超柱是简单知觉的生理基础。
(3)多模式感知细胞：在颞-顶-枕区之间的联络皮层和额叶联络区皮层中，都存在着“多模式感知细胞”，可以对多种信息发生反应，实现着多种感觉的综合反应过程。
多模式感知细胞，是知觉的细胞生理学基础。
(4)总之，皮层中的超柱和联络区皮层多模式感知细胞，在知觉形成中具有重要作用，并可能是知觉的结构和功能单元。
超柱实现同一种感觉模式中，各种属性的综合反应形成简单的知觉;多模式感知细胞则将多种模式的感觉信息综合为复杂的知觉。
2.精神盲：两半球颞下回的损伤使猴不能识别现实刺激物。
它们看见蛇也视而不见，冷若冰霜，失去了正常猴所具有的那种恐惧反应能力。
因而将颞下回损伤造成的这种认知障碍，称为精神盲。
3.多模式感知神经元：颞下回的一些神经元，不仅对复杂视觉刺激物单位发放率增加和发生最大的反应，而且对多种其它感觉刺激，如躯体觉、运动觉、食物嗅觉与味觉等刺激均可引起其单位发放率的变化。
因此，将这类神经元称谓多模式感知神经元。
4.脑事件相关电位中N1波(潜伏期约100毫秒左右负波)，是知觉形成中注意参与水平的客观指标。