主页 > 医学动态 >
[Science/10.29]压力如何影响记忆
研究人员报告说，一个过去被发现与躁郁症和精神分裂症有关的酶，在不同形式的压力下，干涉大鼠和猴子的短期记忆。位于眼睛上面的前额叶皮层是大脑高级执行功能，包括计划和短期或“工作”记忆的必要部位。任何一个经历了特别紧张的一天的人，大概都能证实，压力抑制前额叶的认知功能。Shari Birnbaum和同事现在报告说，一个被称为蛋白质激酶C(PKC)的酶的高度活动破坏了动物的记忆能力。压力能够造成PKC活动的增加，也造成注意力分散、判断力降低、冲动、和思维紊乱，所有这些都与大脑的这个部位有关。作者提出，过剩的PKC活性可能与压力下记忆减弱有关，也可能与其他精神疾病症状有关。
全文见：http://intl.sciencemag.org/cgi/content/abstract/306/5697/882 哇，看来还是要想办法缓解压力才好啊，支持楼主的建议 我认为压力是适度的较好，保持适度的压力，可以提高神经兴奋性，而神经在有和没有一定的兴奋的基础上给予相同的刺激，其反应是不同的，在有兴奋的基础上的刺激，其反应更为强烈。另外神经兴奋还能兴奋循环系统，增加脑部供氧，使思维敏捷，记忆更加深刻。当然了，压力过大就会象笑比哭好兄说的：PKC活动的增加，造成注意力分散、判断力降低、冲动、和思维紊乱。所以生活要有张有驰。 楼上讲的很联系实际。支持一下。 全文rotein Kinase C Overactivity Impairs Prefrontal Cortical Regulation of Working Memory
S. G. Birnbaum,1,2 P. X. Yuan,3 M. Wang,1 S. Vijayraghavan,1 A. K. Bloom,1 D. J. Davis,1 K. T. Gobeske,1 J. D. Sweatt,2 H. K. Manji,3 A. F. T. Arnsten1*
The prefrontal cortex is a higher brain region that regulates thought, behavior, and emotion using representational knowledge, operations often referred to as working memory. We tested the influence of protein kinase C (PKC) intracellular signaling on prefrontal cortical cognitive function and showed that high levels of PKC activity in prefrontal cortex, as seen for example during stress exposure, markedly impair behavioral and electrophysiological measures of working memory. These data suggest that excessive PKC activation can disrupt prefrontal cortical regulation of behavior and thought, possibly contributing to signs of prefrontal cortical dysfunction such as distractibility, impaired judgment, impulsivity, and thought disorder.
1 Department of Neurobiology, Yale Medical School, 333 Cedar Street, New Haven, CT 06520–8001, USA.
2 Department of Neuroscience, 1 Baylor Plaza, Baylor College of Medicine, Houston TX 77030, USA.
3 Laboratory of Molecular Pathophysiology, National Institute of Mental Health (NIMH), Bethesda, MD 20892–4405, USA.
* To whom correspondence should be addressed. E-mail: amy.arnsten@yale.edu
--------------------------------------------------------------------------------
The prefrontal cortex allows us to appropriately guide our behaviors, thoughts, and emotions by using representational knowledge. Lesions of the prefrontal cortex produce symptoms of impulsivity, distractibility, and poor judgment. More extensive disruptions of prefrontal cortical function may also contribute to thought disorder (1) and hallucinations (2, 3). Prefrontal cortical deficits are found in both bipolar disorder (4) and schizophrenia (1), illnesses worsened by exposure to stress (5, 6) and recently associated with changes in PKC intracellular signaling (7–10).
PKC signaling is initiated by activation of phospholipase C releasing diacylglycerol (DAG), which subsequently binds to and activates PKC (Fig. 1A). Phorbol esters such as phorbol 12-myristate 13-acetate (PMA) activate PKC by acting as a long-lasting substitute for DAG (11); chelerythrine (CHEL) inhibits PKC activity by blocking this site. Once activated, PKC translocates from the cytosol to the plasma membrane and other subcellular compartments and undergoes auto-phosphorylation (p-PKC). Alpha-1 adrenergic receptors (1R) are coupled to PKC signaling by Gq proteins; thus, norepinephrine (NE, the endogenous ligand) and phenylephrine (PE, an 1R agonist) indirectly activate PKC (Fig. 1A). We tested whether PMA or 1R stimulation activates PKC in rat prefrontal cortical tissue (10). Because stress exposure increases NE release, activating 1R and impairing prefrontal cortical cognitive function (12), we also examined the effects of the pharmacological stressor FG7142 on PKC activity. PMA, PE, and FG7142 significantly increased PKC activity (range: 23 to 40%, P < 0.05) in the membrane fraction of prefrontal cortical slices (Fig. 1. Simultaneously, cytosolic PKC activity was decreased (range: 12 to 33%). Pretreatment with the PKC inhibitor CHEL completely blocked PMA, PE, or FG7142-induced increases in PKC activity in membranes (Fig. 1. Acute, systemic administration of FG7142 to rats induced a significant increase (36.89% ± 13.5, P < 0.05) in PKC levels (a PKC isoform associated with bipolar disorder; see SOM text) from frontal cortex membrane fractions (Fig. 1C) and a modest but not significant decrease in cytosolic PKC (Fig. 1C), indicating comparable effects in vivo and in vitro.
阅读本文的人还阅读：
作者:admin@医学,生命科学 2011-02-06 17:14
医学,生命科学网