Alterations in hippocampal GAP-43, BDNF, and L1 following sustained cerebral ischemia

Miyake, Kensaku; Yamamoto, Wataru; Tadokoro, M.; Takagi, Norio; Sasakawa, Kyoko; Nitta, Atsumi; Furukawa, Shoei; Takeo, Satoshi

doi:10.1016/s0006-8993(02)02420-4

Cited by 55 publications

(28 citation statements)

References 43 publications

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“…In this model, the penumbral region locates in the hippocampus and there is an increase in the expression of GAP-43 (77). Unfortunately, there is no information as to whether hippocampal plasticity is associated with spontaneous seizures in this model.…”

Section: Cellular Alterationsmentioning

confidence: 99%

Epileptogenesis after Experimental Focal Cerebral Ischemia

et al. 2005

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Cerebrovascular diseases are one of the most common causes of epilepsy in adults, and the incidence of stroke-induced epileptogenesis is increasing as the population ages. The mechanisms that lead to stroke-induced epileptogenesis in a subpopulation of patients, however, are still poorly understood. Recent advances in inducing epileptogenesis in rodent focal ischemia models have provided tools that can be used to identify the risk factors and neurobiologic changes leading to development of epilepsy after stroke. Here we summarize data from models in which epileptogenesis has been studied after focal ischemia; photothrombosis, middle cerebral artery (MCA) occlusion with filament, and endothelin-1-induced MCA occlusion. Analysis of the data indicates that neurobiologic changes occurring during stroke-induced epileptogenesis share some similarities to those induced by status epilepticus or traumatic brain injury.

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Section: Cellular Alterationsmentioning

confidence: 99%

Epileptogenesis after Experimental Focal Cerebral Ischemia

et al. 2005

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“…Moreover, BDNF mRNA levels could be influenced under a variety of pathological conditions known to alter neuronal activity in the brain, including Alzheimer's (Phillips et al 1991;Narisawa-Saito et al 1996;Connor et al 1997;Holsinger et al 2000), ischemia (Lindvall et al 1992;Kokaia et al 1998;Miyake et al 2002), depression (Kokaia et al 1993;Kawahara et al 1997), and stress (Smith et al 1995;Smith and Cizza 1996;Ueyama et al 1997). …”

Section: Activity-dependent Bdnf Transcription and Local Translationmentioning

confidence: 99%

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

Lu¹

2003

Learn. Mem.

842

589

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It is widely accepted that neuronal activity plays a pivotal role in synaptic plasticity. Neurotrophins have emerged recently as potent factors for synaptic modulation. The relationship between the activity and neurotrophic regulation of synapse development and plasticity, however, remains unclear. A prevailing hypothesis is that activity-dependent synaptic modulation is mediated by neurotrophins. An important but unresolved issue is how diffusible molecules such as neurotrophins achieve local and synapse-specific modulation. In this review, I discuss several potential mechanisms with which neuronal activity could control the synapse-specificity of neurotrophin regulation, with particular emphasis on BDNF. Data accumulated in recent years suggest that neuronal activity regulates the transcription of BDNF gene, the transport of BDNF mRNA and protein into dendrites, and the secretion of BDNF protein. There is also evidence for activity-dependent regulation of the trafficking of the BDNF receptor, TrkB, including its cell surface expression and ligand-induced endocytosis. Further study of these mechanisms will help us better understand how neurotrophins could mediate activity-dependent plasticity in a local and synapse-specific manner.Much of the brain's ability to adapt or modify itself in response to experience and environment lies in the plasticity of synaptic connections, both short-and long-terms. Substantial evidence indicates that the number and the strength of synapses can be changed by neuronal activity (Bliss and Collingridge 1993;Linden 1994;Malenka and Nicoll 1999;McEwen 1999). It is now widely accepted that activity-dependent modulation of synapses is critical for brain development as well as many cognitive functions in the adult. Molecular mechanisms that translate patterns of neuronal activity into specific changes in the structures and function of synapses, however, remain largely unknown. A hypothesis was put forward several years ago that neurotrophins may serve as molecular mediators for synaptic plasticity based on two observations: (1) The expression of neurotrophins is regulated by neuroelectric activity; and (2) neurotrophins could modulate the efficacy of synaptic transmission or the growth of dendrites and axons, the structural elements necessary for synaptogenesis

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“…In addition, increased neuronal REST/NRSF Increase in cell migration and cell invasion using matrigel invasion assay [18,20,127] Augmented tumour formation and growth in nude mice [20] L1-dependent gene regulation [20,23,76,132,143] Enhanced resistance to chemotherapy [21,77] Enhanced tumour metastasis formation using spleen-liver mouse model [143] The cell adhesion molecule L1CAM expression has been observed in response to kainateinduced seizures [95] and ischaemia, where REST/NRSF contributes to ischaemia-induced neuronal death [96]. Interestingly, L1 protein expression decreases in the same hippocampal regions following sustained ischaemia [97], suggesting that REST/NRSF may not only repress nonneuronal L1 expression but also acts as a repressor of neuronal L1 expression under pathological conditions. Recently, more than 1,800 genes have been predicted to contain NRSE sites and to represent putative target genes of REST/NRSF [98].…”

Section: Pathological L1cam Gene Regulation In Neurons and Cancermentioning

confidence: 99%

L1CAM malfunction in the nervous system and human carcinomas

Schäfer

Altevogt

2010

Cell. Mol. Life Sci.

131

134

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Research over the last 25 years on the cell adhesion molecule L1 has revealed its pivotal role in nervous system function. Mutations of the human L1CAM gene have been shown to cause neurodevelopmental disorders such as X-linked hydrocephalus, spastic paraplegia and mental retardation. Impaired L1 function has been also implicated in the aetiology of fetal alcohol spectrum disorders, defective enteric nervous system development and malformations of the renal system. Importantly, aberrant expression of L1 has emerged as a critical factor in the development of human carcinomas, where it enhances cell proliferation, motility and chemoresistance. This discovery promoted collaborative work between tumour biologists and neurobiologists, which has led to a substantial expansion of the basic knowledge about L1 function and regulation. Here we provide an overview of the pathological conditions caused by L1 malfunction. We further discuss how the available data on gene regulation, molecular interactions and posttranslational processing of L1 may contribute to a better understanding of associated neurological and cancerous diseases.

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Alterations in hippocampal GAP-43, BDNF, and L1 following sustained cerebral ischemia

Cited by 55 publications

References 43 publications

Epileptogenesis after Experimental Focal Cerebral Ischemia

Epileptogenesis after Experimental Focal Cerebral Ischemia

BDNF and Activity-Dependent Synaptic Modulation: Figure 1.

L1CAM malfunction in the nervous system and human carcinomas

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