Literature DB >> 18323506

Rapid morphologic plasticity of peri-infarct dendritic spines after focal ischemic stroke.

Craig E Brown1, Charles Wong, Timothy H Murphy.   

Abstract

BACKGROUND AND
PURPOSE: Focal stroke is associated with cell death, abnormal synaptic activity, and neurologic impairments. Given that many of these neuropathologic processes can be attributed to events that occur shortly after injury, it is necessary to understand how stroke affects the structure of neurons in surviving peri-infarct regions, particularly at the level of the dendritic spines, which transmit normal and potentially abnormal and injurious synaptic signaling. Recently, we described ischemia-induced changes in the structure of layer 1 dendritic tufts of transgenic mice expressing YFP in layer 5 cortical neurons. However, these in vivo imaging experiments could not address ischemia-related phenomena that occur in deeper cortical structures/layers, other cortical regions, or submicron changes in dendritic spine structure.
METHODS: Focal stroke was induced in the forelimb sensorimotor cortex by the photothrombotic method. Two, 6, and 24 hours after stroke, brains were processed for Golgi-Cox staining to permit a detailed analysis of primary apical dendritic spine structure from layer 2/3 and 5 cortical pyramidal neurons.
RESULTS: Photothrombotic stroke caused a rapid deterioration of neurons, as revealed by Golgi-Cox labeling, in the infarct core that could be readily distinguished from surviving peri-infarct regions. Analysis of >15,000 dendritic spines revealed that although many spines were lost in the peri-infarct cortex during the first 24 hours after stroke (approximately 38% lost), spines that remained were significantly longer (approximately 25% at 6 hours). Furthermore, these effects were found in both layer 2/3 and 5 neurons and were restricted primarily to peri-infarct regions (<200 mum from the infarct border).
CONCLUSIONS: These rapid changes in dendritic spine number and length may reflect an early adaptive response of potentially vulnerable peri-infarct neurons coping with postischemic spreading depression-like depolarizations and the loss of presynaptic contacts.

Entities:  

Mesh:

Year:  2008        PMID: 18323506     DOI: 10.1161/STROKEAHA.107.498238

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  76 in total

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2.  Experimental and preliminary clinical evidence of an ischemic zone with prolonged negative DC shifts surrounded by a normally perfused tissue belt with persistent electrocorticographic depression.

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4.  In vivo voltage-sensitive dye imaging in adult mice reveals that somatosensory maps lost to stroke are replaced over weeks by new structural and functional circuits with prolonged modes of activation within both the peri-infarct zone and distant sites.

Authors:  Craig E Brown; Khatereh Aminoltejari; Heidi Erb; Ian R Winship; Timothy H Murphy
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7.  Selective estrogen receptor modulators (SERMs) enhance neurogenesis and spine density following focal cerebral ischemia.

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9.  Hypoxia-inducible factor 1 contributes to N-acetylcysteine's protection in stroke.

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Review 10.  Inflammatory mechanisms in ischemic stroke: therapeutic approaches.

Authors:  Shaheen E Lakhan; Annette Kirchgessner; Magdalena Hofer
Journal:  J Transl Med       Date:  2009-11-17       Impact factor: 5.531

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