Regulated transcripts in the hippocampus following transections of the entorhinal afferents

Ying, Guo; Liu, Xin; Wang, Wen Yuan; Wang, Yan; Dong, Jing; Jin, Hui; Huang, Cheng; Zhou, Chuanjiang

doi:10.1016/j.bbrc.2004.07.099

“…An upregulation in gelsolin mRNA [331] and gelsolin protein levels [332] was found in the rat hippocampus following entorhinal deafferentation, suggesting that gelsolin may play a role in brain remodeling following hippocampal injury. Filopodia and lamellipodia are enriched with gelsolin [333, 334], and gelsolin knock-out mice exhibit slower filopodial retraction [335], further supporting the role of gelsolin in cell-protrusive activities.…”

Section: Proteins Regulating Actin Dynamics In Dendritic Spinesmentioning

confidence: 99%

Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines

Pontrello

¹

,

Ethell

²

2009

TONEURJ

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Dendritic spines are actin-rich structures that accommodate the postsynaptic sites of most excitatory synapses in the brain. Although dendritic spines form and mature as synaptic connections develop, they remain plastic even in the adult brain, where they can rapidly grow, change, or collapse in response to normal physiological changes in synaptic activity that underlie learning and memory. Pathological stimuli can adversely affect dendritic spine shape and number, and this is seen in neurodegenerative disorders and some forms of mental retardation and autism as well. Many of the molecular signals that control these changes in dendritic spines act through the regulation of filamentous actin (F-actin), some through direct interaction with actin, and others via downstream effectors. For example, cortactin, cofilin, and gelsolin are actin-binding proteins that directly regulate actin dynamics in dendritic spines. Activities of these proteins are precisely regulated by intracellular signaling events that control their phosphorylation state and localization. In this review, we discuss how actin-regulating proteins maintain the balance between F-actin assembly and disassembly that is needed to stabilize mature dendritic spines, and how changes in their activities may lead to rapid remodeling of dendritic spines.

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“…An upregulation in gelsolin mRNA [331] and gelsolin protein levels [332] was found in the rat hippocampus following entorhinal deafferentation, suggesting that gelsolin may play a role in brain remodeling following hippocampal injury.…”

Section: +mentioning

confidence: 96%

Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines

Pontrello¹,

Ethell²

2014

TONEURJ

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Dendritic spines are actin-rich structures that accommodate the postsynaptic sites of most excitatory synapses in the brain. Although dendritic spines form and mature as synaptic connections develop, they remain plastic even in the adult brain, where they can rapidly grow, change, or collapse in response to normal physiological changes in synaptic activity that underlie learning and memory. Pathological stimuli can adversely affect dendritic spine shape and number, and this is seen in neurodegenerative disorders and some forms of mental retardation and autism as well. Many of the molecular signals that control these changes in dendritic spines act through the regulation of filamentous actin (F-actin), some through direct interaction with actin, and others via downstream effectors. For example, cortactin, cofilin, and gelsolin are actin-binding proteins that directly regulate actin dynamics in dendritic spines. Activities of these proteins are precisely regulated by intracellular signaling events that control their phosphorylation state and localization. In this review, we discuss how actin-regulating proteins maintain the balance between F-actin assembly and disassembly that is needed to stabilize mature dendritic spines, and how changes in their activities may lead to rapid remodeling of dendritic spines.

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“…In a differential screening using cDNA microarray analysis for identifying the genes that might be responsible for the lesion-induced plasticity, we have separated a number of genes whose expression levels are upregulated in the rat hippocampus following PP transections, one of which is interferon-␥ receptor (IFN-␥R) (Ying et al, 2004). In the present study, we further analyzed the expression of IFN-␥R mRNA and assayed the mRNA levels of IFN-␥ in the deafferented mouse hippocampus.…”

Section: Introductionmentioning

confidence: 99%

Involvement of interferon-? and its receptor in the activation of astrocytes in the mouse hippocampus following entorhinal deafferentation

Wang

¹

,

Zhou

²

2005

Glia

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The activation of glial cells has been thought to be a universal and important reaction to trauma and pathology in the mammalian central nervous system. The mechanism of glial activation is not completely clear to date, but numerous cytokines have been demonstrated to effectively influence the process in vitro and in vivo. Here we reported the axotomy-induced upregulation of interferon-gamma (IFN-gamma) receptor mRNA in the mouse hippocampus following transections of the entorhinal afferents. Northern blot analysis showed that the transcripts of IFN-gamma receptor were upregulated in a transient manner in the deafferented mouse hippocampus. In situ hybridization confirmed the temporal upregulation of IFN-gamma receptor mRNA specifically in the denervated areas of the mouse hippocampus, which showed that the expression of IFN-gamma receptor mRNA rose slightly at 2 days postlesion, increased remarkably at 3 days postlesion, nearly reached the maximum at 7 days postlesion, and almost returned to control levels at 15 days postlesion. Double labeling further proved that the upregulated IFN-gamma receptor mRNA was confined to reactive astrocytes. At 2 and 3 days postlesion, we also observed the expression of IFN-gamma mRNA by a small number of cells in the denervated areas. We noted that the upregulation of both IFN-gamma and its receptor expression coincided spatiotemporally with astroglial activation, suggesting the potential involvement of IFN-gamma and its receptor in the activation process of astrocytes in the hippocampus following entorhinal deafferentation.

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Regulated transcripts in the hippocampus following transections of the entorhinal afferents

Cited by 6 publications

References 37 publications

Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines

Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines

Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines

Involvement of interferon-? and its receptor in the activation of astrocytes in the mouse hippocampus following entorhinal deafferentation

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