力竭运动前后大鼠脑皮质运动区递质性氨基酸含量的动态变化

通过观察脑递质性氨基酸的变化,进一步探索运动性疲劳的中枢机制,30只雄性SD大鼠进行了一次性力竭跑台运动,用高效液相色谱法检测了运动前后及恢复期：0．5h、1h、3h和24h大鼠脑皮质运动区Glu、Asp、GABA、Gly含量,结果发现：力竭运动后即刻Glu含量有所下降,GABA含量显著性上升至最高点;Gly含量在力竭运动后即刻、恢复0．5、1h均显著性高于安静值,恢复期0．5h达到最高点,同GABA含量变化相比具有时相差异性;Glu／GABA比值在恢复期有所增高,而Glu＋Asp／GABA＋Gly比值始终低于安静值。提示：大鼠脑皮质运动区Glu含量下降和GABA含量增高与运动中枢抑制过程有关;Gly对中枢机能的调控存在复杂的机制;观察大鼠脑中Glu＋Asp／GABA＋Gly比值,反映运动性疲劳时脑的机能状态,较Glu／GABA比值更有意义。     

力竭运动对大鼠脑纹状体5-HT含量及其代谢的影响

目的:观察力竭运动对大鼠脑纹状体5-羟色胺(5-HT)含量及其代谢的影响,分析纹状体中5-HT合成代谢和分解代谢中各指标的关系,进一步探讨力竭运动后脑5-HT含量及其代谢的动态变化对运动性中枢疲劳发生、发展的影响并分析其机理。方法:大鼠分为两组。力竭运动组大鼠进行一次性游泳运动直至力竭。断头处死,取纹状体测色氨酸(Trp)、5-HT和5-羟吲哚乙酸(5-HIAA)含量,测色氨酸羟化酶(TPH)和单胺氧化酶(MAO)活性,取血清测游离色氨酸(f-Trp)含量。结果:与安静组5-HT含量及其代谢各指标相比,力竭运动组大鼠血清f-Trp含量有下降趋势,其余各指标均呈升高趋势,其中纹状体Trp(P<0.01)和5-HIAA(P<0.001)含量显著升高。结论:(1)力竭运动引起血清Trp透过血脑屏障进入脑中增多,导致血清f-Trp含量下降且纹状体Trp含量增多,激活TPH的活性,增强脑5-HT的合成。(2)运动中5-HT的分解也是增加的,说明力竭运动使5-HT代谢加快,易产生中枢疲劳。提示力竭运动组大鼠在力竭运动后,中枢神经系统抑制过程占优势。     

游泳训练及环境应激对大鼠中脑酪氨酸羟化酶与纹状体多巴胺含量的影响

50只SD雄性成年大鼠分别接受不同时间的水应激、一次性力竭游泳运动和长期游泳耐力训练,用免疫印迹法检测中脑TH含量,以荧光发光分析法检测纹状体DA含量。结果显示：长期游泳训练与安静状态的大鼠和一次性力竭游泳大鼠相比中脑TH含量有升高的趋势,但以上变化并没有显著性差异;而一次性力竭游泳运动使得大鼠纹状体DA含量高与安静组,长期游泳耐力训练引起了大鼠纹状体DA含量显著性升高;处于一次性水环境与长期水环境的大鼠中脑TH与纹状体DA含量无显著性差异;长期耐力游泳训练大鼠中脑TH和纹状体DA含量显著性高于处于水环境的大鼠。提示：一次性力竭游泳运动抑制了中脑TH活性,而长期游泳耐力训练有助于提高大鼠中脑TH含量,增加纹状体DA的释放量,提高中枢兴奋性,从而能够改善中枢机能,延迟中枢疲劳的发生时间;水环境会抑制大鼠中脑TH含量,从而使机体处于中枢抑制状态,建议在建立大鼠游泳训练模型中,应增列水环境对照组,从而增强实验的可比性与真实性。     

游泳运动对大鼠纹状体、下丘脑多巴胺的含量及其代谢的影响

目的：探讨游泳运动对大鼠纹状体、下丘脑（DA）内多巴胺的含量及其代谢的影响.方法：选取72只雄性SD大鼠,随机分成6组：安静对照组（A）、一次性力竭游泳运动组（B）、安静＋水环境组（C）、游泳耐力训练组（D）、水环境组（E）、游泳耐力训练后一次性力竭游泳运动组（F）.D组按照耐力训练方案进行负重训练,每周5次,持续7周.所有大鼠一起断头处死,各组交叉进行,迅速取出脑组织（纹状体、下丘脑）进行多巴胺浓度和单胺氧化酶B（MAO-B）活性的测试.结果：一次性力竭运动或游泳训练对下丘脑中DA含量或MAO-B活性的影响无明显影响,而纹状体DA浓度在一次性力竭运动尤其是游泳训练后都明显升高（P〈0.05）,MAO-B也有升高的趋势.结论：一次性力竭运动尤其是游泳耐力训练使DA的浓度和MAO-B活性增加,其合成和分解代谢都增加,提高了DA的转换率,以适应运动的需要,有利于改善脑机能,延缓运动疲劳,是适应运动的表现.     

沙苑子对运动训练大鼠骨骼肌自由基代谢的影响

通过建立力竭跑台训练模型,测试大鼠骨骼肌组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性、谷胱甘肽过氧化物酶(GSH-Px)活性、丙二醛(MDA)含量和ATP酶活性,探讨沙苑子对力竭跑台训练大鼠骨骼肌组织自由基代谢、ATP酶活性和运动能力的影响.结果显示,与安静组比较,运动力竭组SOD、CAT和GSH-Px活性降低,MDA含量升高;沙苑子组大鼠骨骼肌组织活性显著高于对照组,MDA含量明显低于相应对照组(P<0.01);运动力竭组Na 、K -ATPase和Ca2 、Mg2 -ATPase活性与安静组比较降低,沙苑子组大鼠骨骼肌组织ATPase活性显著高于对照组.沙苑子可显著提高运动大鼠抗氧化的功能,提高运动大鼠骨骼肌组织ATPase活性,具有较强抗氧化能力,使大鼠运动能力有了明显提高.     

隔药灸神阙对耐力训练再力竭运动大鼠心肌、骨骼肌自由基代谢的影响

以SD大鼠为研究对象,建立耐力训练再力竭运动大鼠模型,通过测定不同组别大鼠心肌、骨骼肌中SOD、CAT、GSH-Px活性及MDA含量的变化,探讨隔药灸神阙对耐力训练再力竭运动大鼠心肌、骨骼肌自由基代谢的影响.结果显示,训练隔药灸组大鼠心肌、骨骼肌中SOD、CAT、GSH-Px活性均显著高于训练组(P<0.05),GSH-Px活性与安静组比较无差异(P>0.05);MDA含量显著低于训练组(P<0.05),与安静组比较无差异(P>0.05).由此提示,隔药灸神阙可减轻耐力训练再力竭运动对大鼠心肌、骨骼肌造成的脂质过氧化损伤,改善运动造成的机体自由基代谢紊乱,从而明显延长耐力训练大鼠力竭时间.     

槲皮素对运动训练大鼠肝组织自由基代谢及运动能力影响实验研究

通过对大鼠在安静状态、非力竭运动状态及力竭运动状态下肝组织中总超氧化物歧化酶(T—SOD)、铜锌超氧化物歧化酶(CuZn—SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性及丙二醛(MDA)含量的测定，分析了槲皮素对运动训练大鼠肝组织自由基代谢及运动能力的影响．结果表明，槲皮素对运动训练大鼠肝组织产生的自由基具有清除效果和保护作用，可减少运动后因脂质过氧化产生的内源性自由基对机体的损伤，保护细胞膜的完整性，从而增强抗氧化酶活力．提高大鼠运动能力．     

女贞子提取物对大鼠肾组织氧化损伤的保护作用及对运动能力的影响

研究女贞子提取物对大强度耐力训练大鼠肾组织抗氧化酶活性和自由基代谢的影响,探讨女贞子提取物对大鼠运动能力的作用机制.6周后,对安静对照组在安静时,力竭运动组和力竭运动加药组进行一次力竭运动后取材,测定肾组织总超氧化物歧化酶活性(T-SOD)、铜锌超氧化物歧化酶(Cu,Zn-SOD)、锰超氧化物歧化酶(Mn-SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)等抗氧化酶活性和谷胱甘肽(GSH)、丙二醛(MDA)的质量含量.结果表明,力竭运动加药组,大鼠肾组织抗氧化酶活性与力竭运动组比较均有显著升高(P<0.05);力竭运动加药组大鼠肾组织GSH的质量含量显著高于力竭运动组(P<0.05),力竭运动加药组肾组织MDA的质量含量显著低于力竭运动组(P<0.05).力竭运动加药组大鼠运动至力竭时间比力竭运动组延长23.09%.说明补充女贞子提取物可以调节大鼠肾组织中抗氧化酶活性,增加GSH的质量含量,减少MDA的生成,延长运动至疲劳的时间.     

佛手水提液对大强度运动训练大鼠物质代谢及运动能力的影响

研究了佛手水提液对大强度运动训练大鼠体内物质代谢及运动能力的影响.以训练大鼠为实验对象,灌胃给药不同剂量的佛手水提液28 d,每日进行游泳力竭训练,测定训练结束后的大鼠血睾酮、皮质酮、尿素氮等生理指标.结果显示佛手水提液具有延长训练大鼠力竭时间(P0.01)、缓解运动所致血清睾酮下降(P0.01)、增加肝肌糖原储备(P0.05)和降低尿素氮含量(P0.01)、提高血红蛋白水平(P0.01)等作用,可提升运动机能和耐力,最终达到改善和抵抗运动性疲劳的目的.     

脑组织中5-HT及受体与运动的研究现状

运用文献资料法,系统地概括了脑内5-羟色胺（5-hydroxytryptamine,5-HT）及其受体的特性,并总结了近年来脑内5-HT及受体与运动的研究现状：1．5-HT作为一种抑制性神经递质可以降低从中枢向外周发放的冲动,导致中枢疲劳。2．5-HT的升高可能首先发生在某一脑区而非全脑。3．耐力运动中大脑5-HT含量升高且在疲劳时加剧。4．力竭运动可同时加快5-HT的合成和降解速度,脑内5-HT在运动即刻几乎没有明显变化。5．5-HT受体各亚型存在较大差异,有的起抑制性作用,有的则发挥兴奋性作用。     

Reduction in number of immunostained GABAergic neurones in deprived-eye dominance columns of monkey area 17

The primary visual cortex (area 17) of the Old World monkey is divided into alternating right- and left-eye dominance columns that are highly modifiable by visual experience during a critical period in development but display little morphological or physiological plasticity during adult life. However, changes in immunocytochemical staining for a calcium/calmodulin-dependent protein kinase occur in visual cortical neurones of adult monkeys after brief monocular deprivation and concentrations of putative neurotransmitters or their related enzymes can be altered with changes in neuronal activity in other systems. We therefore examined the effects of monocular deprivation on the immunocytochemical staining for gamma-aminobutyric acid (GABA) and its synthetic enzyme, glutamic acid decarboxylase (GAD), in adult monkey area 17. The staining for GABA and GAD in neuronal somata and terminals was markedly reduced within ocular dominance columns associated with a removed or a visually deprived eye, suggesting that the GABA concentration in cortical neurones may depend on their levels of activity. Thus area 17 of adult monkeys may retain a greater degree of plasticity than previously recognized and sensory experience can profoundly affect transmitter levels, in the cortex, apparently by regulating levels of a synthetic enzyme.     

Inhibitory neurones of a motor pattern generator in Xenopus revealed by antibodies to glycine

Glycine and gamma-aminobutyric acid (GABA) are inhibitory transmitters of major importance. Whereas neurones using GABA as the transmitter can be visualized by immunocytochemical methods for glutamate decarboxylase (GAD) or GABA, no comparable techniques have been available for the selective visualization of glycinergic neurones. We have now produced polyclonal antibodies which specifically recognize glycine in glutaraldehyde-fixed tissue. We used these antibodies to investigate the distribution of glycine in the simple central nervous system (CNS) of the Xenopus embryo, which contains an anatomically and physiologically defined class of reciprocal inhibitory interneurones, the commissural interneurones. These interneurones have an important role in the generation of the swimming motor pattern and are thought to be glycinergic. The glycine antibodies specifically stain these interneurones, revealing their distribution and number in the embryo CNS. This is the first demonstration of the selective localization of glycine-like immunoreactivity in a putative glycinergic class of neurone that has been characterized physiologically, pharmacologically and anatomically.     

GABA may be a neurotransmitter in the vertebrate peripheral nervous system

gamma-Aminobutyric acid (GABA) is an inhibitory neurotransmitter in the peripheral nervous system of certain invertebrates and is thought to be a major transmitter in the vertebrate central nervous system. In this report we present evidence that GABA may also be a neurotransmitter in the vertebrate peripheral autonomic nervous system. We have used light and electron microscopic autoradiography to analyse high-affinity uptake of 3H-GABA into the myenteric plexus of the guinea pig taenia coli, both in situ and in a tissue culture preparation. In the isolated myenteric plexus, we have measured the specific activity of glutamic acid decarboxylase (GAD; EC 4.1.1.15), the enzyme responsible for conversion of glutamic acid to GABA in GABAergic neurones, and assessed the ability of this tissue to accumulate 3H-GABA newly synthesised from 3H-glutamic acid. Furthermore, we have measured the levels of endogenous GABA in strips of taenia coli containing the myenteric plexus.     

Analgesia and hyperalgesia from GABA-mediated modulation of the cerebral cortex

It is known that pain perception can be altered by mood, attention and cognition, or by direct stimulation of the cerebral cortex, but we know little of the neural mechanisms underlying the cortical modulation of pain. One of the few cortical areas consistently activated by painful stimuli is the rostral agranular insular cortex (RAIC) where, as in other parts of the cortex, the neurotransmitter gamma-aminobutyric acid (GABA) robustly inhibits neuronal activity. Here we show that changes in GABA neurotransmission in the RAIC can raise or lower the pain threshold--producing analgesia or hyperalgesia, respectively--in freely moving rats. Locally increasing GABA, by using an enzyme inhibitor or gene transfer mediated by a viral vector, produces lasting analgesia by enhancing the descending inhibition of spinal nociceptive neurons. Selectively activating GABA(B)-receptor-bearing RAIC neurons produces hyperalgesia through projections to the amygdala, an area involved in pain and fear. Whereas most studies focus on the role of the cerebral cortex as the end point of nociceptive processing, we suggest that cerebral cortex activity can change the set-point of pain threshold in a top-down manner.     

氨基酸代谢、脑神经递质与运动性中枢疲劳

运动性疲劳的机制主要包括存在于大脑的中枢机制和肌肉本身的外周机制两个方面,越来越多的证据表明,氨基酸代谢、脑神经递质与中枢疲劳有着密切关系,对色氨酸、谷氨酸和酷氨酸代谢;脑神经递质;脑神经递质5－羟色胺、r-氨基丁酸和多巴胺及其与运动性中枢疲劳的关系作一简要综述。     

GABA affects the release of gastrin and somatostatin from rat antral mucosa

gamma-Aminobutyric acid (GABA) is regarded as the major inhibitory neurotransmitter in the central nervous system of vertebrates. GABA exerts its inhibitory actions by interacting with specific receptors on pre- and postsynaptic membranes and has been shown to inhibit somatostatin release from hypothalamic neurones in vitro. Concepts of innervation of the gastrointestinal tract have been expanded by recent studies which suggest that GABAergic neurones are not confined solely to the central nervous system but may also exist in the vertebrate peripheral autonomic nervous system. Jessen and coworkers have demonstrated the presence, synthesis and uptake of GABA by the myenteric plexus of the guinea pig taenia coli, and have documented the presence of glutamic acid decarboxylase (GAD) in isolated myenteric plexus. This enzyme is responsible for the conversion of glutamic acid to GABA in GABAergic neurones. The possibility that GABA may have a role in neurotransmission or neuromodulation in the enteric nervous system of the vertebrate gut has been suggested by several investigators. Furthermore, GABA receptors have been demonstrated on elements of the enteric nervous system. The effects of GABA on gastrointestinal endocrine cell function have not been examined. We report here the effects of GABA on gastrin and somatostatin release from isolated rat antral mucosa in short-term in vitro incubations.     

药物对小白鼠不同脑区GABA_A受体与外源性GABA_A结合的影响

用同位素示踪法测定药物对小鼠四个不同脑区的GABA_A受体与外源性GABA结合的影响。GABA_A受体颉颃剂Picrotoxin,bicuculline,青霉素,和GABA-T抑制剂AOAA均使大脑皮层的受体结合显著增加,中枢兴奋剂戊四唑使之显著地减少。AOAA使海马的受体结合显著增加,戊四唑及安定使之显著减少。蝎毒使下丘脑的受体结合显著增加,而戊四唑使之显著减少。AOAA、蝎毒、bicuculline、picrotoxin使小脑的受体结合显著增加。     

五味子多糖和游泳运动对疲劳大鼠中枢神经系统的影响

通过对大鼠的分组对照实验,研究了五味子多糖和游泳运动对疲劳大鼠大脑皮层自由基代谢的影响.实验表明,适宜的游泳运动和五味子多糖可以防止力竭大鼠大脑皮层缺血缺氧所导致的脂质过氧化,清除自由基危害,延缓大鼠中枢神经疲劳的出现.     

Inhibitory threshold for critical-period activation in primary visual cortex

Neuronal circuits across several systems display remarkable plasticity to sensory input during postnatal development. Experience-dependent refinements are often restricted to well-defined critical periods in early life, but how these are established remains mostly unknown. A representative example is the loss of responsiveness in neocortex to an eye deprived of vision. Here we show that the potential for plasticity is retained throughout life until an inhibitory threshold is attained. In mice of all ages lacking an isoform of GABA (gamma-aminobutyric acid) synthetic enzyme (GAD65), as well as in immature wild-type animals before the onset of their natural critical period, benzodiazepines selectively reduced a prolonged discharge phenotype to unmask plasticity. Enhancing GABA-mediated transmission early in life rendered mutant animals insensitive to monocular deprivation as adults, similar to normal wild-type mice. Short-term presynaptic dynamics reflected a synaptic reorganization in GAD65 knockout mice after chronic diazepam treatment. A threshold level of inhibition within the visual cortex may thus trigger, once in life, an experience-dependent critical period for circuit consolidation, which may otherwise lie dormant.