Density and morphology of dendritic spines in mouse neocortex

Ballesteros-Yáñez, Inmaculada; Benavides-Piccione, Ruth; Elston, Guy N.; Yuste, Rafael; DeFelipe, Javier

doi:10.1016/j.neuroscience.2005.11.038

Cited by 130 publications

(103 citation statements)

References 40 publications

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“…Similar to a report by Ballesteros-Yanez et al, 31 control apical dendritic spine density levels ( Figure 2C) for the primary motor (9.61Ϯ1.0 spines/10 m), secondary motor (8.21Ϯ0.6 spines/10 m), and contralateral barrel (9.18Ϯ0.6 spines/10 m) cortex did not differ significantly from one another (F 2,12 ϭ0.98, Pϭ0.40). However, within 24 hours after stroke, spine density levels dropped significantly in the Figure 1.…”

Section: Resultssupporting

confidence: 90%

Rapid Morphologic Plasticity of Peri-Infarct Dendritic Spines After Focal Ischemic Stroke

Brown

Wong

Murphy

2008

Stroke

163

110

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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 Ͼ15 000 dendritic spines revealed that although many spines were lost in the peri-infarct cortex during the first 24 hours after stroke (Ϸ38% lost), spines that remained were significantly longer (Ϸ25% at 6 hours). Furthermore, these effects were found in both layer 2/3 and 5 neurons and were restricted primarily to peri-infarct regions (Ͻ200 m from the infarct border). Key Words: neuronal plasticity Ⅲ penumbra Ⅲ excitotoxicity Ⅲ focal cerebral ischemia Ⅲ mice Ⅲ recovery T he sudden loss of blood flow to the brain (ie, ischemia) causes an immediate loss of cells in the ischemic core that is surrounded by an area of compromised, but potentially salvageable, tissue known as the penumbra, or peri-infarct region. 1 Because of this potential for rejuvenation, investigations have examined the physiologic changes that take place within the peri-infarct region during the first few hours and days after stroke. 2 For example, it is known that ischemia and reperfusion rapidly induce the production of reactive oxygen species, mitochondrial dysfunction, and glutamate release that is followed by repetitive spreading depression-like depolarizations and changes in intra-and extracellular loads of electrolytes (ie, calcium, potassium, zinc). 2-4 These abrupt changes in neuronal excitability and ionic homeostasis during the early stages of stroke could conceivably lead to extensive changes in the structure of peri-infarct neurons that may significantly affect their survival. Indeed, in vitro studies of oxygen/glucose deprivation or in vivo models of global ischemia have described acutely dysmorphic dendritic processes, spine loss, and filopodial formation within minutes of ischemia. [5][6][7] Recent ...

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Section: Resultssupporting

confidence: 90%

Rapid Morphologic Plasticity of Peri-Infarct Dendritic Spines After Focal Ischemic Stroke

Brown

Wong

Murphy

2008

Stroke

163

110

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“…Brain sections (100 m) including the dorsal hippocampus were obtained using a vibratome (VT-1000S, Leica) and stained with DAPI (Sigma). With the aid of a micromanipulator, individual neurons were injected by microiontophoresis with Lucifer yellow (8% in 0.1 M Tris buffer, pH 7.4) (Elston and Rosa, 1997;Benavides-Piccione et al, 2002;Ballesteros-Yáñez et al, 2006). The microcapillary containing the neuronal tracer was backfilled with LiCl (0.1 M).…”

Section: Stereotaxis and Immunohistochemistrymentioning

confidence: 99%

“…PTD4-rhodamine was used both as a control of spine density and to monitor peptide diffusion in control animals. After 72 h, experimental and control animals were killed, and their brains were processed for Lucifer yellow tracer microinjection and counterstained with an antibody against Lucifer yellow to enhance the signal (Elston and Rosa, 1997;Benavides-Piccione et al, 2002;Ballesteros-Yáñez et al, 2006) (Fig. 7A; supplemental Fig.…”

Section: Pi3k Induces Spinogenesis In Adult Neuronsmentioning

confidence: 99%

Phosphoinositide-3-Kinase Activation Controls Synaptogenesis and Spinogenesis in Hippocampal Neurons

Cuesto

Enriquez-Barreto²,

Caramés³

et al. 2011

J. Neurosci.

125

129

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The possibility of changing the number of synapses may be an important asset in the treatment of neurological diseases. In this context, the synaptogenic role of the phosphoinositide-3-kinase (PI3K) signaling cascade has been previously demonstrated in Drosophila. This study shows that treatment with a PI3K-activating transduction peptide is able to promote synaptogenesis and spinogenesis in primary cultures of rat hippocampal neurons, as well as in CA1 hippocampal neurons in vivo. In culture, the peptide increases synapse density independently of cell density, culture age, dendritic complexity, or synapse type. The induced synapses also increase neurotransmitter release from cultured neurons. The synaptogenic signaling pathway includes PI3K-Akt. Furthermore, the treatment is effective on adult neurons, where it induces spinogenesis and enhances the cognitive behavior of treated animals in a fear-conditioning assay. These findings demonstrate that functional synaptogenesis can be induced in mature mammalian brains through PI3K activation.

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“…The second source of heterogeneity occurs on a much longer length scale that is comparable to the length of a dendrite, which can vary from 100 µm to a few millimeters. The latter heterogeneity reflects the experimental observation that there is a slow proximal to distal variation in the density of spines (Konur et al 2003;Ballesteros-Yanez et al 2006). In this paper, we analyze how both sources of heterogeneity modulate the speed of CaMKII translocation waves along a spiny dendrite.…”

Section: Introductionmentioning

confidence: 93%

“…In particular, we took the homogenized translocation rate h to be constant over the length of a dendrite. However, it is found experimentally that there is a slow proximal to distal variation in the density of spines (Konur et al 2003;Ballesteros-Yanez et al 2006). An illustration of a typical spine density found in pyramidal neurons of mouse cortex (Ballesteros-Yanez et al 2006) is shown in Fig.…”

Section: Wavespeed For a Slowly Modulated Spine Densitymentioning

confidence: 99%

Propagation of CaMKII translocation waves in heterogeneous spiny dendrites

Bressloff

2012

J. Math. Biol.

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CaMKII (Ca 2+ -calmodulin-dependent protein kinase II) is a key regulator of glutamatergic synapses and plays an essential role in many forms of synaptic plasticity. It has recently been observed experimentally that stimulating a local region of dendrite not only induces the local translocation of CaMKII from the dendritic shaft to synaptic targets within spines, but also initiates a wave of CaMKII translocation that spreads distally through the dendrite with an average speed of order 1µm/s. We have previously developed a simple reaction-diffusion model of CaMKII translocation waves that can account for the observed wavespeed and predicts wave propagation failure if the density of spines is too high. A major simplification of our previous model was to treat the distribution of spines as spatially uniform. However, there are at least two sources of heterogeneity in the spine distribution that occur on two different spatial scales. First, spines are discrete entities that are joined to a dendritic branch via a thin spine neck of submicron radius, resulting in spatial variations in spine density at the micron level. The second source of heterogeneity occurs on a much longer length scale and reflects the experimental observation that there is a slow proximal to distal variation in the density of spines. In this paper, we analyze how both sources of heterogeneity modulate the speed of CaMKII translocation waves along a spiny dendrite. We adapt methods from the study of the spread of biological invasions in heterogeneous environments, including homogenization theory of pulsating fronts and Hamilton-Jacobi dynamics of sharp interfaces.

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Density and morphology of dendritic spines in mouse neocortex

Cited by 130 publications

References 40 publications

Rapid Morphologic Plasticity of Peri-Infarct Dendritic Spines After Focal Ischemic Stroke

Rapid Morphologic Plasticity of Peri-Infarct Dendritic Spines After Focal Ischemic Stroke

Phosphoinositide-3-Kinase Activation Controls Synaptogenesis and Spinogenesis in Hippocampal Neurons

Propagation of CaMKII translocation waves in heterogeneous spiny dendrites

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