2011年自学考试生理心理学串讲笔记第四章
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04年10月《生理心理学》串讲笔记1-自学考试(△为填空题、□为选择题、◎名词解释、☆为问答题、★重点题)导论(整章△、□、◎)一、神经解剖学知识(重点掌握)△、□、◎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。
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。
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。
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。
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。
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。
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。
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。
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。
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。
尾状核与豆状核组成纹状体,对机体的运动功能具有调节作用。
间脑位于大脑与中脑之间,被大脑两半球所遮盖,由丘脑、上丘脑、下丘脑和底丘脑四大部分组成。
丘脑是皮层下除嗅觉外所有感觉的重要整合中枢。
《生理心理学》串讲笔记(二)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。
超柱仅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;联络区皮层的多模式感知细胞,则将多种模式的感觉信息综合为复杂的知觉。
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。
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。
第四章注意注意并不是一个独立的心理过程,只不过是一种心理状态,是某种心理活动的指向性、选择性、集中性。
这种心理活动可能是感知过程,也可思维过程,所以,注意总是和认知活动同时存在。
◎朝向反应就是由这种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。
朝向反应是非随意注意的生理基础。
经典神经生理学家巴甫洛夫在狗唾液条件反射实验中发现,对于已经建立起唾液条件反射的狗,给予一个突然意外的新异性声音刺激,则唾液分泌条件反射立即停止,狗将头转向声源方向,两耳竖起,两眼凝视瞳孔散大,四肢肌肉紧张,心率和呼吸变慢,动物作出应付危险的准备。
巴甫洛夫认为这种对新异刺激的朝向反射本质是脑内发展了外抑制过程。
新异刺激在脑内产生的强兴奋灶对其他脑区发生明显的负诱导,因而抑制了已建立的条件反射活动。
随着新异刺激的重复呈现,失去了它的新异性,在脑内逐渐发展了消退抑制过程,抑制了引起朝向反射的兴奋灶,于是朝向反射不复存在。
由此可见,巴甫洛夫关于朝向反射的理论主要是根据动物的行为变化,概括出脑内抑制过程的变化规律,用他的神经过程及其运动规律加以解释。
2021年自考“生理心理学”串讲资料第四章第四章注意注意:并不是一个独立的心理过程,只不外是一种心理状态,是某种心理活动的指向性、选择性、集中性。
这种心理活动可能是感知过程,也可思维过程,所以,注意总是和认知活动同时存在,还常伴有情绪体验和情绪表示。
(名词解释)朝向反应:就是由一种新异性强刺激引起机体的一种反射活动,表示为机表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标的目的。
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。
朝向反应是非随意注意的生理基础。
经典神经生理学家巴甫洛夫在狗唾液条件反射实验中发现:对于已经建立起唾液条件反射的狗,给予一个突然不测的新异性声音刺激,则唾液分泌条件反射立即停止,狗将头转向声源标的目的,两耳竖起,两眼凝视瞳孔散大,四肢肌肉紧张,心率和呼吸变慢,动物作出应付危险的准备。
巴甫洛夫认为这种对新异刺激的朝向反射本质是脑内发展了外按捺过程。
新异刺激在脑内产生的强兴奋灶对其他脑区发生明显的负诱导,因而按捺了已建立的条件反射活动。
随着新异刺激的重复呈现,失去了它的新异性,在脑内逐渐发展了消退按捺过程,按捺了引起朝向反射的兴奋灶,于是朝向反射不复存在。
由此可见,巴甫洛夫关于朝向反射的理论主要是按照动物的行为变化,概括出脑内按捺过程的变化规律,用他的神经过程及其运动规律加以解释。
具体地讲,脑内发展的外按捺是朝向反射形成的机制,而主动性内按捺过程――消退按捺的产生引起朝向反射的消退。
(重点题)(问答题)索科洛夫的朝向反应及如何解释(匹配理论)索科洛夫在朝向反应的研究中发现,它是一个包罗许多脑结构在内的复杂功能系统。
这一功能系统的最显著特点是它在新刺激作用下形成的新异刺激模式与神经系统的活动模式之间的不匹配,是这种反应的生理基础。
具体地讲,这种机制发生在对刺激信息反应的传出神经元中,在这里将感觉神经元传入的信息模式和中间神经元保留的以前刺激痕迹的模式加以匹配,如果两个模式完全匹配,传出神经元不再发生反应。
2011年自考生理心理学串讲笔记 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。
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,研究并揭示心理现象产生过程中有机体的生理活动过程、特别是中枢神经系统和它的高级部位——大脑的活动方式,是生理心理学的主要任务。
3.研究生理心理学的意义:第一,生理心理学为科学心理学的建立作出了重要贡献。
它在解释心理的实质方面有着不可替代的作用。
随着新的研究成果的不断涌现,这门学科对心理科学的发展必将继续产生重要影响。
第二,人类的科学事业正在面临着物质的本质、宇宙的起源、生命的本质和智力的产生四大问题的挑战。
这四大问题的最后一个,也是最困难的一个:智力是如何由物质产生的,正是心理科学研究的主要问题之一。
研究智力的产生,生理心理学是可以大有作为的。
第三,生理心理学的研究成果能够为高新技术的发展提供好的思路。
第四,研究生理心理学的巨大动力和这门学科的生命力,还在于它是对人类自身的心理活动进行寻根究底的。
第五,生理心理学能够为许多实践领域服务,尤其是为人类的医疗卫生事业服务。
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),并且能改变体内化学物质的含量。
●分子遗传学技术:原理:基因控制化学物质的合成。
●脑成像技术:定义:通过成像技术记录脑活动的部位和功能变化。
分为结构成像和功能成像。
单光子发射计算机断层扫描、正电子发射计算机断层扫描、功能性核磁共振成像、核磁共振波谱、脑电图、事件相关电位、CT、PET。
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。
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. [3]S.D.Anker and S.Von Haehling,“Inflammatory mediators inchronic heart failure:an overview,”Heart,vol.90,no.4,pp.464–470,2004.[4]J.Or´us,E.Roig,F.Perez-Villa et al.,“Prognostic value of serumcytokines in patients with congestive heart failure,”Journal of Heart and Lung Transplantation,vol.19,no.5,pp.419–425, 2000.[5]M.Rauchhaus,W.Doehner,D.P.Francis et al.,“Plasmacytokine parameters and mortality in patients with chronic heart failure,”Circulation,vol.102,no.25,pp.3060–3067, 2000.[6]A.Deswal,N.J.Petersen,A.M.Feldman,J.B.Y oung,B.G.White,and D.L.Mann,“Cytokines and cytokine receptors in advanced heart failure:an analysis of the cytokine database from the Vesnarinone Trial(VEST),”Circulation,vol.103,no.16,pp.2055–2059,2001.[7]S. 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 Rehabilitation,vol.13,no.4,pp.592–597,2006.[25]rsen,K.B.Helle,M.Christensen,J.T.Kvaloy,T.Aars-land,and K.Dickstein,“Effect of exercise training on chro-mogranin A and relationship to N-ANP and inflammatory cytokines in patients with chronic heart failure,”International Journal of Cardiology,vol.127,no.1,pp.117–120,2008.[26]outaris,A.Dritsas,M.D.Brown et al.,“Immuneresponse to inspiratory muscle training in patients with chronic heart failure,”European Journal of Cardiovascular Pre-vention and Rehabilitation,vol.14,no.5,pp.679–685,2007.[27]J.Niebauer,A.L.Clark,k.M.Webb-Peploe,and A.J.Coats,“Exercise training in chronic heart failure:effects on pro-inflammatory markers,”European Journal of Heart Failure, vol.7,no.2,pp.189–193,2005.[28]N.Smart,“Effects of exercise training on functional capacity,quality of life,cytokine and brain natriuretic peptide levels in hart failure patients,”Journal of Medical and Biological 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0410月《生理心理学》串讲笔记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。
超柱仅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;联络区皮层的多模式感知细胞,则将多种模式的感觉信息综合为复杂的知觉。
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。
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。
第四章注意
注意并不是一个独立的心理过程,只不过是一种心理状态,是某种心理活动的指向性、选择性、集中性。
这种心理活动可能是感知过程,也可思维过。
2011年自学考试生理心理学资料串讲笔记四
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,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。
★☆眼睛的随意运动有哪几种方式?它的生理心理学意义是什么?
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。
人们在观察客体时,有意识地使眼睛进行这些运动,以便使物像能最好地投射在视网膜上最灵敏的部位――中央窝上,得到最清楚的视觉。
☆非随意的眼动
★☆微颤的生理心理学意义是什么?什么是适应现象?
在两次扫视之间,眼球不动,称注视,其持续时间约在150-400毫秒之间。
注视期间,眼睛并非绝对不动;事实上此时眼睛发生快速微颤。
微颤运动保证视网膜不断变换感受细胞对注视目标进行反映,从而克服了每个光感受细胞由于适应机制而引起的感受性降低。
颜色视觉信息的光生物化学基础
△□光生物化学反应主要发生在视杆细胞之中,是产生明暗视觉信息的基础。
颜色视觉的光生物化学基础在于视锥细胞内的视蛋白结构不同。
视网膜上有哪几种细胞?排列方式及电传导方式。
△□◎☆
□视网膜分为内、外两层。
外层是色素上皮层,由色素细胞组成,由此产生和储存一些光化学物质。
内层是由5种神经细胞组成的神经层,从外向内依次为视感受细胞(视杆细胞和视锥细胞)、水平细胞、双极细胞、无足细胞和神经节细胞。
细胞联系的一般规律是几个视感受细胞与1个双极细胞联系,几个双极细胞又与1个神经节细胞相关。
因此,多个视感受细胞只引起1个神经节细胞兴奋,故视敏度较差;但在视网膜中央凹部只有视锥细胞,每个视锥细胞只与1个双极细胞相联系,而这个双极细胞又与1个神经节细胞相联系。
因此,中央凹视敏度最高。
由视感受细胞、双极细胞和神经节细胞形成神经信息传递的垂直联系;由水平细胞和无足细胞在垂直联系之间进行横向联系,1个神经节细胞及与其相互联系的全部其他视网膜细胞,构成视觉的最基本结构与功能单位,称之为视感受单位。
视网膜中央凹附近的视感受单位较小,而周边部分视网膜的感受单位较大。
除了神经节细胞之外,视网膜上的其他细胞对光刺激的反应均类似光感受细胞,根据光的相对强度变化给出级量反应,这种级量反应是缓慢的电变化,不能形成可传导的动作电位,但可与邻近细胞的慢变化发生时间和空间总和效应。
水平细胞和无足细胞对视觉信息横向联系的作用正是以慢电位变化的总和效应为基础的。
在视网膜上对光刺激的编码,只有神经节细胞才类似于脑内其他神经元,产生单位发放,对刺激强度按调频的方式给出神经编码。
视网膜的横向联系中,水平细胞和无足细胞对信息的处理和从光感受细胞至双极细胞间的信息传递都是以级量反应为基础的模拟过程,只有神经节细胞的信息传递才是全或无的数字化过程。
视觉的传导通路:始于视网膜上的神经节细胞,其细胞轴突构成视神经,末梢止于外侧膝状体。
来自两眼鼻侧的视神经左右交叉到对侧外侧膝状体;而来自两眼颞侧的视神经,不发生交叉投射到同侧外侧膝状体。
外侧膝状体细胞发出的纤维经视放射投射至大脑皮层的初级视皮层(V1),继而与二级(V2)、三级(V3)和四级(V4)。
等次级视皮层发生联系。
V1区与简单视感觉有关,V2区与图形或客体的轮廓或运动感知有关,V4区主要与颜色觉有关。
★☆神经节细胞、外侧膝状体、皮层神经元感受野有什么不同?
视网膜神经节细胞的感受野呈现同心圆式,其中心区和周边区之间总是拮抗的。
外侧膝状体神经元的感受野与神经节细胞基本相似,形成中心区和周边区相互拮抗的同心圆式的感受野。
皮层神经元的感受野分三种类型:简单型、复杂型、超复杂型。
简单型感受野面积较小,引起开反应和闭反应的区均呈直线型,两者分离形成平行直线,但两者可以存在空间总和效应;
复杂型感受野较简单型大,呈长方形且不能区分出开反应与闭反应区,可以看成是由直线型简单感受野平行移动而成,也可以看成是大量简单型皮层细胞同时兴奋而造成的;
超复杂型感受野的反应特性与复杂型相似,但有明显的终端抑制,即长方形的长度超过一定限度则有抑制效应。
总之,简单型的细胞感受野是直线形,与图形边界线的觉察有关;复杂型和超复杂型细胞为长方形感受野,与对图形的边角或运动感知觉有关。
◎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。
□人能听到频谱大约为20—16000赫兹的各种声波,对400—1000赫兹的声波最敏感。
物理声学分析声音的频率、振幅或声压以及复合声的频谱;心理声学考虑到这些参数与人类主观听觉间的关系,则提出相应的参数是音高、音强和音色。
听觉通路:耳蜗核-内侧膝状体,由内侧膝状体将听觉信息传送到颞叶的初级听皮层(41区)和次级听皮层(21区,22区,42区)
□听觉信息的神经编码(理论):德国黑尔姆霍兹听觉共振假说;位置理论;频率理论;美国贝克西行波学说。
△关于内耳音高编码问题的两种方式为细胞分工编码和频率编码。
□△在外周和中枢内对音强编码的机制较为复杂,可分为极量反应式编码、调频式编码、细胞分工编码。
□生源空间定位的神经编码有两种基本方式:锁相-时差编码,强度差编码。
味觉通路:舌的味觉传入冲动均达脑干孤束核,在这里交换神经元后上行至桥脑味觉区,最后达大脑皮质的前岛叶,这里是最高级味觉中枢。
嗅觉通路:前梨状区及杏仁核内侧。
躯体感觉模式及编码的一般规律
躯体的感觉模式是多种多样的,我们可以将它们由表及里分成三个层次:浅感觉、深感觉、内脏感觉。
浅感觉包括触觉、压觉、振动觉、温度感觉等,这些感受细胞都分布在皮肤中;深感觉是对关节、肢体位置、运动及受力作用的感觉,它们的感受细胞分布在关节、肌肉、肌腱等组织中;内脏感觉一般情况下这些感觉并不投射到意识中来,分布在脏器、血管壁之中,受到牵拉或触压会引起痛觉。
躯体感觉神经编码的基本规律是对各种刺激模式进行细胞分工编码,而这些细胞又以不同空间对应关系分布着;对于刺激强度则以神经元单位发放频率的改变进行编码。
躯体内外的各种刺激,按其刺激性质引起相应感受细胞的兴奋。
转自:<a href='/zxks/'>育路自学考试网</a>。