首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   765篇
  国内免费   15篇
  完全免费   26篇
  神经病学   806篇
  2018年   10篇
  2017年   11篇
  2016年   8篇
  2015年   7篇
  2014年   11篇
  2013年   22篇
  2012年   19篇
  2011年   16篇
  2010年   22篇
  2009年   19篇
  2008年   32篇
  2007年   33篇
  2006年   23篇
  2005年   69篇
  2004年   47篇
  2003年   13篇
  2002年   20篇
  2001年   21篇
  1999年   13篇
  1998年   17篇
  1997年   25篇
  1996年   19篇
  1995年   14篇
  1994年   14篇
  1993年   14篇
  1992年   26篇
  1991年   20篇
  1990年   17篇
  1989年   21篇
  1988年   12篇
  1987年   10篇
  1986年   23篇
  1985年   26篇
  1984年   32篇
  1983年   24篇
  1982年   26篇
  1981年   28篇
  1980年   15篇
  1979年   2篇
  1978年   3篇
  1977年   1篇
  1973年   1篇
排序方式: 共有806条查询结果,搜索用时 42 毫秒
1.
Karen Gale 《Epilepsia》1988,29(S2):S15-S34
Summary: Seizure activity is generated and propagated by specific subcortical circuits. The substantia nigra (SN) and the area tempestas (AT) have been identified as two exemplary substrates for the control of experimental seizures. In animal models, GABAergic transmission has been shown to protect against seizures of different origins and methods of induction. Neuroactive peptides and excitatory amino acids may work with GABA in the SN to control the propagation of a wide variety of seizure types. In contrast, inhibition of AT pons selectively protects against seizures associated with limbic circuits. The AT is also a site from which bilaterally synchronous convulsions can be triggered in response to manipulations of cholinergic, GABAergic, and excitatory amino acid receptors. Definition of other pathways of seizure development and the effects of pharmacologic treatments on discrete brain regions await further research efforts.  相似文献
2.
Cajal was probably the first neurobiologist to suggest that plasticity of nerve cells almost completely disappeared during aging. However, we know today that neural plasticity is still present in the brain during aging. In this review we suggest that aging is a physiological process that occurs asynchronously in different areas of the brain and that the rate of that process is modulated by environmental factors and related to the neuronal-synaptic-molecular substrates of each area. We review here some of the most recent results on aging of the brain in relation to the plastic changes that occur in young and aged animals as a result of living in an enriched environment. We highlight the results from our own laboratory on the dynamics of neurotransmitters in different areas of the brain. Specifically we review first the effects of aging on neurons, dendrites, synapses, and also on molecular and functional plasticity. Second, the effects of environmental enrichment on the brain of young and aged animals. And third the effects of an enriched environment on the age-related changes in neurogenesis and in the extracellular concentrations of glutamate and GABA in hippocampus, and on dopamine, acetylcholine, glutamate and GABA under a situation of acute mild stress in the prefrontal cortex.  相似文献
3.
James O. McNamara 《Epilepsia》1989,30(S1):S13-S18
Summary: The greatest value of the kindling model for new therapy of epilepsy almost certainly lies in elucidating the molecular basis of its development and persistence. Such an understanding may provide a foundation for therapies aimed at prevention or perhaps even cure of some forms of human epilepsy.  相似文献
4.
H. Steve White 《Epilepsia》1997,38(S1):S9-S17
Summary: More than 50 million persons worldwide suffer from epilepsy, many of whom are refractory to treatment with standard antiepileptic drugs (AEDs). Fortunately, new AEDs commercialized since 1990 are improving the clinical outlook for many patients. Our growing understanding of anticonvulsant mechanisms and the relevance of preclinical animal studies to clinical antiepileptic activity have already contributed to the design of several new AEDs and should be increasingly beneficial to further efforts at drug development. Mechanisms have been identified for older AEDs [phenytoin (PHT), carbamazepine (CBZ), valproate (VPA), barbiturates, benzodiazepines (BZDs), ethosuximide (ESM)] and newer AEDs [vigabatrin (VGB), lamotrigine (LTG), gabapentin (GBP) tiagabine (TGB), felbamate (FBM), topiramate (TPM)]. Several novel anticonvulsant mechanisms have recently been discovered. FBM appears to be active at the strychnine-insensitive glycine binding site of the NMDA receptor. TPM is active on the kainate/AMPA subtype of glu-tamate receptor and at a potentially novel site on the GABAA receptor. For several reasons, availability of a single AED with multiple mechanisms of action may be preferred over availability of multiple AEDs with single mechanisms of action. These reasons include ease of titration, lack of drug-drug interactions, and reduced potential for pharmacodynamic tolerance.  相似文献
5.
GABA in Epilepsy: The Pharmacologic Basis   总被引:5,自引:5,他引:1  
Karen Gale 《Epilepsia》1989,30(S3):S1-S11
Summary: GABA transmission plays a key role in controlling seizure activity. The precise nature of its effect depends on the particular location in the brain and the pathway involved. Animal studies have helped to define specific brain regions such as the substantia nigra and area tempestas that are critical in controlling seizure activity. Antiepileptic drugs such as vigabatrin [gamma vinyl GABA (GVG)], a drug rationally developed to treat resistant epilepsy, can enhance GABA transmission in these regions and may thereby afford seizure protection.  相似文献
6.
Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.  相似文献
7.
GABAergic Mechanisms in Epilepsy   总被引:5,自引:5,他引:27  
8.
New Antiepileptic Drugs: From Serendipity to Rational Discovery   总被引:4,自引:4,他引:3  
Summary: Antiepileptic drug discovery has made enormous progress from the serendipity and screening processes of earlier days to the rational drug development of today. The modern era of research began with the recognition that enhancement of inhibitory processes in the brain might favorably influence the propensity for seizures, γ-aminobutyric acid (GABA) being the main inhibitory transmitter. Work in this field led to the development of vigabatrin, which inhibits the enzyme responsible for the degradation of GABA. More recently, research has focused on the therapeutic potential of blocking excitatory amino acids—in particular glutamate. Of the three receptors for glutamate, the N-methyl- d -aspartate (NMDA) receptor is considered the one of most interest in epilepsy, and research on a series of competitive NMDA receptor antagonists—especially those that are orally active—is in the forefront of antiepileptic drug development today. A further alternative for diminishing neuronal excitability is to modulate sodium, potassium, or calcium channels. The latter are especially implicated in absence seizures.
Antiepileptic drug discovery has evolved from serendipity through random screening to a scientific era where drugs are designed rationally according to modern principals of neuroscience and the art of medicinal chemistry. Of the research directions currently being pursued, the following appear to be particularly promising: enhancement of inhibition, reduction in excitation, and modulation of the ionic channels that are the fundamental mediators of neuronal excitability. The application of modern approaches to drug discovery provides some optimism that effective new compounds will be marketed in the coming decade, with the promise of diminished suffering by persons with uncontrolled epilepsy.  相似文献
9.
Antiepileptic Drug Mechanisms of Action   总被引:4,自引:4,他引:4  
Summary: Clinically used antiepileptic drugs (AEDs) decrease membrane excitability by interacting with ion channels or neurotransmitter receptors. Currently available AEDs appear to act on sodium channels, GABAA receptors, or calcium channels. Phenytoin, carbamazepine, and possibly valproate (VPA) decrease high-frequency repetitive firing of action potentials by enhancing sodium channel inactivation. Benzodiazepines and barbiturates enhance GABAA receptor-mediated inhibition. Ethosuximide and possibly VPA reduce a low-threshold calcium current. The mechanisms of action of AEDs currently under development are less clear. Lamotrigine may decrease sustained high-frequency repetitive firing. The mechanisms of action of felbamate are unknown. Gabapentin (GBP) appears to bind to a specific binding site in the central nervous system with a restricted regional distribution, but the identity of the binding site and the mechanism of action of GBP remain uncertain.  相似文献
10.
OBJECTIVE: Among antipsychotics, clozapine ranks highest in terms of the risk for weight gain and developing diabetes. However, the mechanism by which clozapine induces weight gain and diabetes remains unclear. The aim of this study was to determine the mechanism of clozapine-induced weight gain and hyperglycemia, and to clarify whether clozapine-induced hyperglycemia results from impairment of the system regulating appetite. METHODS: Circulatory glucose, insulin, leptin and ghrelin levels were analyzed after acute administration of clozapine in rats. Clozapine (10 mg/kg) or a vehicle was injected intraperitoneally and blood samples were collected at 0, 15, 30, and 60 min after the injection. Clozapine (5, 10 or 20 mg/kg) or the vehicle was given, and blood samples were collected at 30 min after the injection. Since clozapine has receptor affinity for multiple neurotransmitters, selective antagonists of it, including dopamine, serotonin, alpha-adrenergic, muscarine and histamine were administered to clarify the pathway of clozapine-induced blood glucose and changes in plasma ghrelin. RESULTS: Clozapine administration increased the blood glucose level at all time points (p<0.05) compared to controls. Plasma ghrelin was elevated at 30 min (p=0.0124) and 60 min (p=0.00152). Blood glucose was increased in rats given 5 (p=0.0344), 10 (p<0.0001), or 20 mg/kg (p<0.0001) clozapine, while plasma ghrelin was increased in rats treated with 10 mg/kg (p=0.0009) or 20 mg/kg (p=0.0059) clozapine. Blood glucose was increased in rats treated with a selective alpha1-adrenergic receptor antagonist (p<0.0001), while plasma ghrelin was significantly increased in rats given a selective alpha1- (p=0.025) or alpha2-adrenergic receptor antagonist (p=0.0003). CONCLUSIONS: Clozapine impairs glucose metabolism and the appetite-regulation system. Clozapine increases blood glucose independent of insulin. The antagonistic action of alpha-adrenergic receptors is one of the mechanisms that induces both hyperglycemia and elevation of ghrelin.  相似文献
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号