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Titlebook: Emerging Strategies in Neuroprotection; Paul J. Marangos,Harbans Lal Book 1992 Birkh?user Boston 1992 Evolution.biology.brain.neuroscience

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發(fā)表于 2025-3-21 17:21:35 | 只看該作者 |倒序瀏覽 |閱讀模式
書目名稱Emerging Strategies in Neuroprotection
編輯Paul J. Marangos,Harbans Lal
視頻videohttp://file.papertrans.cn/309/308382/308382.mp4
叢書名稱Advances in Neuroprotection
圖書封面Titlebook: Emerging Strategies in Neuroprotection;  Paul J. Marangos,Harbans Lal Book 1992 Birkh?user Boston 1992 Evolution.biology.brain.neuroscience
描述SOLOMON H. SNYDER Receptor Research Reaches Neurology: Relevance to Neurodegenerative Diseases and Stroke President George Bush has heralded the 1990s as the decade of the brain, based largely on the rapid escalation of advances in the molecular neuro- sciences and the likelihood that these will bear therapeutic fruit before the turn of the century. There is little doubt that the 1970s and 1980s have witnessed more remarkable advances in the molecular neurosciences than all of the preceding hundred years. Identification of receptor sites for drugs and neurotransmitters along with simple, sensitive, and specific means of monitoring them has made it possible to elucidate the mechanism of action for many known drugs and to identify new chemical entities as potential therapeutic agents. At the same time, the numbers of distinct neurotrans- mitters have multiplied. Prior to 1970 only the biogenic amines were well accepted as transmitters. The early 1970s witnessed the gradual acceptance ofamino acids as major excitatory and inhibitory neurotransmitters. Identification of opiate receptors and the subsequent identification of the enkephalins as their endogenous ligands led to an appreciat
出版日期Book 1992
關(guān)鍵詞Evolution; biology; brain; neuroscience; receptor
版次1
doihttps://doi.org/10.1007/978-1-4684-6796-3
isbn_softcover978-1-4684-6798-7
isbn_ebook978-1-4684-6796-3
copyrightBirkh?user Boston 1992
The information of publication is updating

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Modeling Neurodegeneration and Neuroprotection in Hippocampal Slicestechnique became a useful tool in the hands of electrophysiologists and pharmacologists. Yamamoto and McIlwain (1966) were the first to show that mammalian brain (prepyriform cortex) slices maintained in vitro exhibited electrical activity comparable to that obtained in vivo. Along with cell culture
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Stroke Models for Preclinical Trials of Neuroprotective Agentsain during or following ischemic insult. Despite the numerous claims of therapeutic success in animal models in the past two decades, no therapeutic agents have been approved by the Food and Drug Administration (FDA) for patients with acute ischemic stroke in the United States (Pulsinelli and Buchan
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Animal Models of Ischemiaficulty determining whether a proposed therapy is effective. Appropriate studies in patients are complex, and few animal models are adequate for realistic and efficient tests of pharmacologic methods to reduce damage or restore neurologic function. Most cerebral stroke models have not been designed
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Calcium Channel Blockers and Neuroprotectionolved within a short period of time (minutes), will lead to a core of severely ischemic tissue that may not be salvaged. However, the ultimate size of the brain infarct also depends on the “penumbra,” a zone of tissue around the core of the infarct where blood flow is still maintained above a neuron
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Self-Defense of the Brain: Adenosinergic Strategies in Neurodegenerationedicine. The breadth and scope of the pathologic factors are such that, even with the improved understanding of the involved events, it is extremely difficult to decide which of them are the primary instigators of the ensuing damage and which are but secondary effects of an ongoing process of the ne
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