2011年10月自考《生理心理学》必背知识8
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
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. AcknowledgmentThis work is supported in part by an MBF Research Grant Award2003and a scholarship from the National Heart Foundation of Australia.References[1]J.Niebauer,“Inflammatory mediators in heart failure,”Inter-national Journal of Cardiology,vol.72,no.3,pp.209–213, 2000.[2]S.Gielen,V.Adams,S.M¨o bius-Winkler et al.,“Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure,”Journal of the American College of Cardiology,vol.42,no.5,pp.861–868,2003. 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D.Anker,W.Steinborn,and S.Strassburg,“Cardiaccachexia,”Annals of Medicine,vol.36,no.7,pp.518–529, 2004.[8]rsen,S.Lindal,P.Aukrust,I.Toft,T.Aarsland,and K.Dickstein,“Effect of exercise training on skeletal musclefibre characteristics in men with chronic heart failure.Correlation between skeletal muscle alterations,cytokines and exercise capacity,”International Journal of Cardiology,vol.83,no.1,pp.25–32,2002.[9]D.Tousoulis,M.Charakida,and C.Stefanadis,“Inflammationand endothelial dysfunction as therapeutic targets in patients with heart failure,”International Journal of Cardiology,vol.100,no.3,pp.347–353,2005.[10]S.Ichihara,Y.Yamada,G.Ichihara et al.,“Attenuation ofoxidative stress and cardiac dysfunction by bisoprolol in an animal model of dilated cardiomyopathy,”Biochemical and Biophysical Research Communications,vol.350,no.1,pp.105–113,2006.[11]O.Parodi,R.De Maria,and E.Roubina,“Redox state,oxida-tive stress and endothelial dysfunction in heart failure:the puzzle of nitrate-thiol interaction,”Journal of Cardiovascular Medicine,vol.8,no.10,pp.765–774,2007.[12]S.Adamopoulos,J.Parissis,D.Karatzas et al.,“Physical train-ing modulates proinflammatory cytokines and the soluble Fas/soluble Fas ligand system in patients with chronic heart failure,”Journal of the American College of Cardiology,vol.39, no.4,pp.653–663,2002.[13]S.Adamopoulos,J.T.Parissis,and D.T.Kremastinos,“Newaspects for the role of physical training in the management of patients with chronic heart failure,”International Journal of Cardiology,vol.90,no.1,pp.1–14,2003.[14]S.Adamopoulos,J.Parissis,C.Kroupis et al.,“Physical train-ing reduces peripheral markers of inflammation in patients with chronic heart failure,”European Heart Journal,vol.22, no.9,pp.791–797,2001.[15]ani,vie,and M.R.Mehra,“Reduction inC-reactive protein through cardiac rehabilitation and exercise training,”Journal of the American College of Cardiology,vol.43, no.6,pp.1056–1061,2004.[16]V.M.Conraads,P.Beckers,J.Bosmans et al.,“Combinedendurance/resistance training reduces plasma TNF-αreceptor levels in patients with chronic heart failure and coronary artery disease,”European Heart Journal,vol.23,no.23,pp.1854–1860,2002.[17]J.P.LeMaitre,S.Harris,K.A.A.Fox,and M.Denvir,“Changein circulating cytokines after2forms of exercise training in chronic stable heart failure,”American Heart Journal,vol.147, no.1,pp.100–105,2004.[18]D.Xu,B.Wang,Y.Hou,H.Hui,S.Meng,and Y.Liu,“Theeffects of exercise training on plasma tumor necrosis factor-alpha,blood leucocyte and its components in congestive heart failure patients,”Zhonghua Nei Ke Za Zhi,vol.41,no.4,pp.237–240,2002.[19]L.W.E.Sabelis,P.J.Senden,R.Fijnheer et al.,“Endothelialmarkers in chronic heart failure:training normalizes exercise-induced vWF release,”European Journal of Clinical Investiga-tion,vol.34,no.9,pp.583–589,2004.[20]N.Smart and T.H.Marwick,“Exercise training for patientswith heart failure:a systematic review of factors that improve mortality and morbidity,”American Journal of Medicine,vol.116,no.10,pp.693–706,2004.[21]A.Ferraz,E.A.Boochi,R.S.Meneghelo,I.I.Umeda,andN.Salvarane,“High sensitive C-reactive protein is reduced by exercise training in chronic heart failure patients:a prospective,randomized,controlled study,”Circulation,vol.110,pp.793–794,2004.[22]rsen,P.Aukrust,T.Aarsland,and K.Dickstein,“Effectof aerobic exercise training on plasma levels of tumor necrosis factor alpha in patients with heart failure,”American Journal of Cardiology,vol.88,no.7,pp.805–808,2001.[23]S.Adamopoulos,A.J.Coats,F.Brunotte et al.,“Physicaltraining improves skeletal muscle metabolism in patients with chronic heart failure,”Journal of the American College of Cardiology,vol.21,no.5,pp.1101–1106,1993.[24]A.I.Karavidas,K.G.Raisakis,J.T.Parissis et al.,“Functionalelectrical stimulation improves endothelial function and reduces peripheral immune responses in patients with chronic heart failure,”European Journal of Cardiovascular Prevention and 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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。
自考《心理学》知识点汇总
心理学是一门以解释、预测和调控人的行为为目的，通过研究分析人的行为，揭示人的心理活动规律的科学。
二.实验法在控制条件下对某种行为或者心理现象进行观察的方法称为实验法。
三.不随意注意不随意注意是指事先没有目的、也不需要意志努力的注意。
四.日节律日节律在人和动物身上都存在，它的主要表现为睡与醒的周期性循环，此外，也还有一些生理方面的节律变化，如血压、排尿、荷尔蒙分泌等。
五.随意注意随意注意是指有预定目的，需要一定意志努力的注意，它是一种积极、主动的注意形式。
六.晕轮效应晕轮效应指人们对他人的认知判断首先主要是根据个人的好恶得出的，然后再从这个判断推论出认知对象的其他品质的现象。
七、短时记忆短时记忆也称工作记忆，是信息加工系统的核心。
在感觉记忆中经过编码的信息，进入短时记忆后经过进一步的加工，再从这里进入可以长久保存的长时记忆。
八、发现学习发现学习是在缺乏经验传授的条件下，个体自己去独立发现、创造经验的过程。
通过主客观的相互作用，在主体头脑内部积累经验、构建心理结构以积极适应环境的过程，它可以通过行为或行为潜能的持久变化而有所表现。
十.推理推理是指从一组具体事物经过分析综合得出一般规律，或者从一般原理演出新的具体结论的思维活动。
前者叫归纳推理，后者叫演绎推理。
十一、问题解决在认知心理学中，可以把问题解决定义为具有一系列目标指向性的认知操作。
十二、发散思维发散思维是指人们根据当前问题给定的信息和记忆系统中存储的信息，沿着不同的方向和角度思考，从多方面寻求多样性答案的一种思维活动。
十三、概念概念在心理学上指的是反映客观事物共同特点与本质属性的思维形式，是高级认知活动的基本单元，以一个符号，就是词的形式来表现。
十四、定势在连续进行工作时，如果一个人屡次成功地以相同的方法解决了某类问题，会使他机械性地或盲目地以原有的方式方法解决类似问题，而不去寻求新的、更好的方法。
这种坚持使用原有已证明有效的方法解决新问题的心理倾向，这就是心向或心理定势。
生理心理学 自考 期末考试笔记
第一章导论一、神经解剖学知识A.生理心理学是心理学、神经科学、和信息科学之间的边缘学科。
B脑研究的6个理论体系：自然哲学理论、机能定位理论、经典神经生理学理论、细胞神经生理学理论、脑化学通路学说、神经科学理论。
1.神经解剖将神经系统分为两大部分：即中枢神经系统和外周神经系统。
2.中枢神经系统由颅腔里的脑和椎管内的脊髓组成。
颅腔里的脑又可分为大脑、小脑、间脑、中脑、桥脑和延脑六个脑区。
椎管内的脊髓分31节。
3.外周神经系统是中枢发出的纤维，由12对脑神经和31对脊神经组成，它们分别传递躯干、头、面部的感觉与运动信息。
在脑、脊神经中都有支配内脏运动的纤维，分布于内脏、心血管和腺体，称之为植物神经（自主神经）。
根据植物神经的中枢部位、形态特点，可将其分为交感神经和副交感神经，在功能上彼此拮抗，共同调节和支配内脏活动。
4.神经组织学根据脑与脊髓内的细胞聚集和纤维排列将其分为灰质、白质、神经核和纤维束。
灰质和神经核是由神经细胞体和神经细胞树突组成。
白质和纤维束是由神经细胞的轴突（神经纤维）组成。
5.在大脑中，灰质分布在表层，称为大脑皮层；白质在深部，称为髓质。
在脊髓中正好相反，灰质在内，白质在外。
根据大脑皮层细胞层次不同，可将皮层分为古皮层、旧皮层和新皮层（占大脑皮层90％）。
6.根据解剖部位从前向后，又可将大脑皮层分为额叶、顶叶、枕叶和颞叶。
颞叶以听觉功能为主。
枕叶以视觉功能为主。
顶叶为躯体感觉的高级中枢。
额叶以躯体的运动功能为主。
7.前额叶皮层和颞、顶、枕皮层之间的联络区则与复杂知觉、注意和思维过程有关。
8.边缘叶：大脑的底面与大脑半球内侧缘的皮层－边缘叶（包括胼胝体下回、扣带回、海马回及其海马回深部的海马结构）。
9.边缘系统：边缘叶及皮层下一些脑结构，如丘脑、乳头体、中脑被盖等，共同构成边缘系统，具有内脏脑之称，是内脏功能和机体内的高级调节控制中枢，也是情绪、情感的调节中枢。
10.在大脑髓质（白质）深部有一些神经核团，称基底神经节，包括尾状核、豆状核、杏仁核和屏状核。
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2011年10月自考《生理心理学》必背知识8
第八章本能与动机的生理心理学基础
1.渴中枢——下丘脑前外测区。
饥——下丘脑外侧区，饱中枢——旁室核和围穹窿区。
性反射的初级中枢——脊髓腰段，雄性动物性行为中枢——性两形核，雌性动物性行为中枢——下丘脑的腹内侧核，两性动物的性行为还受更高级的脑中枢调节，颞叶皮层在性对象的识别和选择中发挥重要作用。
颞叶损伤的人或动物均表现出严重的性功能异常。
2.情绪性攻击行为——动物种属内个体间为了争夺食物、领地或性对象而引起的攻击行为。
这些行为的共同特点是带有情绪色彩，所以有时称之为情绪性攻击行为。
①母性攻击行为——与保护自身的生存无关，这是一种保存和延续种族的本能行为。
哺乳期的动物为保护幼仔不受外来者的侵害，以猛烈地攻击驱逐外来者。
②杀幼行为——是将幼仔杀死的行为。
杀幼行为也是对种族延续有利的行为，雄性动物只有杀掉哺乳中的幼仔，才能使雌性动物较早地摆脱哺乳期而重新受孕。
雌性动物的杀幼行为可能与幼仔多、过于拥挤或哺乳能力所不及引起的。
母动物总是选择最弱小仔动物除掉以保证有强壮的后代延续种族。
3.根据杏仁核群的生理功能核系统发生等级，可将其分成两组结构：皮层内侧核和杏仁基外侧核。
4.下丘脑——防御攻击行为的重要中枢;①对于情绪性攻击行为，基外杏仁核发生兴奋性调节作用，隔区产生抑制性调节作用;②对于捕食攻击行为，皮层内侧杏仁核实现着抑制性调节作用。
5.人类睡眠的种类及特点：
人类的睡眠可以分为两种类型：慢波睡眠和异相睡眠。
(1)在慢波睡眠中，脑电活动以慢波为主，脑电活动的变化与行为变化相平行，从入睡期至深睡期，脑电活动逐渐变慢并伴随着逐渐加深的行为变化，表现为肌张力逐渐减弱，呼吸节律和心率逐渐变慢。
(2)在异相睡眠中，脑电变化与行为变化相分离，脑电活动类似慢波睡眠的入睡期，以肌张力为代表的行为变化却比深睡期还深，肌张力完全丧失，还伴有快速眼动现象和桥脑-膝状体-枕叶PGO波周期性高幅放电等特殊变化。
异相睡眠又常称为快速眼动睡眠。
这种类型的睡眠与做梦的关系比慢波睡眠更为密切。
(3)慢波睡眠分为四个发展时期：①睡眠一期(入睡期)，开始进入睡眠状态，清醒安静状态下的脑电活动(以8-13次/秒的α节律为主)。
②睡眠二期(浅睡期)，脑电活动更不规则。
被试已经入睡，并出现鼾声，但将其叫醒后自称没睡着。
③慢波睡眠三期(中睡期)，被试已经睡熟，但尚易叫醒。
④睡眠四期(深睡期)，不但睡熟还难以叫醒，被唤醒后报告做梦者人数极少，但梦魇或恶梦惊醒者多。
生长激素分泌的高峰在慢波睡眠的四期。
(4)在慢波睡眠之后，常出现异相睡眠。
此期睡眠者肌肉呈完全松弛状态，甚至肌肉电活动完全消失，睡眠深度似乎比慢波四期更深，体温仍较低，对外部刺激的感觉功能进一步降低，难以将睡眠者从此期立即唤醒。
与行为变化相反，脑电活动为极不规律的低幅快波。
在异相睡眠中，最有特征的行为变化是眼球快速运动，约每分钟60次左右。
从异相睡眠中唤醒后，80%以上的人声称正在做梦，梦境形象生动，以视觉变幻为主。
(5)人的每夜睡眠大约由慢波睡眠和异相睡眠交替变换4-6个周期所组成，平均每个周期历时80-90分钟，包括20-30分钟异相睡眠和约60分钟的慢波睡眠。
成人入睡后，必须先经过慢波睡眠1-4期和4-2期的顺序变化后，才能进入第一次异相睡眠。
从上半夜到下半夜每次更替一个周期，异相睡眠的时间都有所增长。
所以，后半夜睡眠中，异相睡眠时间的比例增大。
6.PGO波(06名)：在异相睡眠中，最有特征性的行为变化是眼球快速运动，约每分钟6 0次左右，故异相睡眠又常称快速眼动睡眠。
与之相应，眼电现象显著加强，在桥脑、外侧膝状体—枕叶皮层中可记录到周期性的高幅放电现象，称之为PGO波。
发作性睡病、猝倒、入睡前幻觉是异相睡眠中常见的障碍。
夜游症、梦游症、夜惊症是慢波睡眠常见的障碍。
7.睡眠的功能：
(1)睡眠不仅对维持种族延续和个体生存具有同等重要意义。
睡眠还有促进生长发育、易学习、形成记忆等多种功能。
(2)睡眠过程中脑垂体分泌的生长激素增高，在整夜睡眠的第一个慢波睡眠4期出现时达到高峰，随后生长激素沿血液循环达全身各处发挥生理作用。
这恰好处于慢波睡眠4期之后的异相睡眠期。
躯体组织各种细胞，特别是儿童骨骼细胞迅速分裂，蛋白质合成率也相应地迅速增加。
说明睡眠有助于未成年机体的生长发育。
(3)异相睡眠总蛋白质合成率增加与睡眠之前受到各种刺激的信息编码和记忆储存有关。
对整夜睡眠的梦分析表明，每夜睡眠中第一二两次异相睡眠的梦多以重现白天的活动内容为主，似乎对当天经历进行着重新整理核编码;第三四两次异相睡眠的梦多重复过去的经历甚至是儿时的体验;第五次异相睡眠的梦既有近事记忆又有往事记忆的内容。
⑷这些事实似乎支持异相睡眠中蛋白质合成增加与信息编码、短时记忆以及长时记忆储存有关。
有人认为儿童期接触很多新事物，需要编码和储存的信息较多，睡眠较多;老年人需要学习内容减少，睡眠也减少。
8.脑干网状结构在睡眠与觉醒中的重要作用
(1)60年代对睡眠机制的认识水平。
①脑干以上横断脑(孤立脑标本)——在中脑四叠体的上丘和下丘之间横断猫脑，动物陷入永久睡眠状态;②脑干中间横断脑(桥脑中部横断)——动物70-90%时间处于觉醒状态;③脑干下位横断脑(孤立头标本)——在脊髓和延脑之间横断，动物维持正常的睡眠与觉醒周期。
证明在延脑至中脑的脑干中，存在着调节睡眠与觉醒的脑中枢。
④脑干上部的网状上行激活系统对维持觉醒状态起重要作用;桥脑下部的网状结构对睡眠起重要作用;脑干上部与下部的网状结构相互作用维持正常的睡眠与觉醒周期。
(2)70年代以来对睡眠机制的研究积累了相当多的科学事实，证明脑内存在着一些关键性结构，其生理、生化过程的维持与转换对睡眠具有重要作用。
①慢波睡眠的关键性脑结构：缝际核、孤束核和视前区、前脑基底部;②异相睡眠的关键性脑结构：桥脑大细胞区(“开细胞”)、蓝斑中小细胞(“闭细胞”)、外侧膝状体神经元(记录外侧外侧膝状体内PGO波的差异，可很快预测异相睡眠时眼动的方向)和延脑网状大细胞核等;③与睡眠有关的化学物质：单胺类、胆碱类和多肽等神经递质，特别是诱导睡眠肽和氨基丁酸受体蛋白。
(3)最近20年对于睡眠与觉醒周期的生物钟的研究取得较大的成果，认识到下丘脑的视交叉上核起着重要的作用。