Automatic Dendritic Spine Quantification from Confocal Data with Neurolucida 360

Dickstein, Dara L.; Dickstein, Daniel R.; Janssen, William G.M.; Hof, Patrick R.; Glaser, Jack R.; Rodríguez, Alfredo; O'Connor, Nate; Angstman, P. J.; Tappan, Susan

doi:10.1002/cpns.16

Cited by 80 publications

(80 citation statements)

References 46 publications

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“…Images of 40 μm‐thick sections were acquired, with z‐step 0.25 μm, using a 60x oil immersion objective (numerical aperture 1.4; pixel size, 0.23 x 0.23 μm) as described in our previous study (Gisabella et al, ). For dendritic spine quantification, confocal microscopy images were analyzed using Neurolucida 360 software with Autospine to measure spine density in apical and basal dendrites of hippocampus CA1 pyramidal cells and their secondary branches using an approach previously described (Dickstein et al, ; Rodriguez, Ehlenberger, Dickstein, Hof, & Wearne, ). Dendritic spines were sampled from proximal and distal dendrites, in both primary and secondary branches by an investigator who was blinded to the treatment group of the animals.…”

Section: Methodsmentioning

confidence: 99%

Regulation of hippocampal dendritic spines following sleep deprivation

Gisabella

Scammell

Bandaru

et al. 2019

J of Comparative Neurology

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Section: Methodsmentioning

confidence: 99%

Regulation of hippocampal dendritic spines following sleep deprivation

Gisabella

Scammell

Bandaru

et al. 2019

J of Comparative Neurology

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“…Z-stack images at 0.1μm intervals were acquired in the molecular layer of the dentate gyrus under a 63x oil objective with a five-time digital zoom (pixel size = 57.21nm, NA = 1.44, resolution = 512x512, frame average = 4) and were then deconvolved using Autoquant software (RRID:SCR_002465). Z-stacks of dendritic fragments were then visualized in three dimensions using Neurolucida 360 (RRID:SCR_001775) [44], 10μm dendritic fragments were randomly selected for spine counting (no more than one fragment per dendrite) and analyzed by a blinded experimenter. To avoid underestimation of the spine PLOS ONE density that could be due to spherical aberrations over the Z axis, spine counts were expressed relative to fragment lengths [45].…”

Section: Neuronal Morphological Analysismentioning

confidence: 99%

Apolipoprotein E regulates the maturation of injury-induced adult-born hippocampal neurons following traumatic brain injury

Tensaouti

Kernie

2020

PLoS ONE

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Various brain injuries lead to the activation of adult neural stem/progenitor cells in the mammalian hippocampus. Subsequent injury-induced neurogenesis appears to be essential for at least some aspects of the innate recovery in cognitive function observed following traumatic brain injury (TBI). It has previously been established that Apolipoprotein E (ApoE) plays a regulatory role in adult hippocampal neurogenesis, which is of particular interest as the presence of the human ApoE isoform ApoE4 leads to significant risk for the development of late-onset Alzheimer's disease, where impaired neurogenesis has been linked with disease progression. Moreover, genetically modified mice lacking ApoE or expressing the ApoE4 human isoform have been shown to impair adult hippocampal neurogenesis under normal conditions. Here, we investigate how controlled cortical impact (CCI) injury affects dentate gyrus development using hippocampal stereotactic injections of GFP-expressing retroviruses in wild-type (WT), ApoE-deficient and humanized (ApoE3 and ApoE4) mice. Infected adult-born hippocampal neurons were morphologically analyzed once fully mature, revealing significant attenuation of dendritic complexity and spine density in mice lacking ApoE or expressing the human ApoE4 allele, which may help inform how ApoE influences neurological diseases where neurogenesis is defective.

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“…Images of dendritic spines were captured and analyzed as previously described (51). The investigator was blinded to treatment group.…”

Section: Iontophoretic Dye Injection Neuronal Imaging 3-dimensionalmentioning

confidence: 99%

Repeated hypoglycemia blunts the responsiveness of glucose-inhibited GHRH neurons by remodeling neural inputs and disrupting mitochondrial structure and function

Bayne

Alvarsson

Devarakonda

et al. 2019

Preprint

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Hypoglycemia is a frequent complication of diabetes, limiting therapy and increasing morbidity and mortality.With recurrent hypoglycemia, the counter-regulatory response (CRR) to decreased blood glucose is blunted, resulting in hypoglycemia unawareness. The mechanisms leading to these blunted effects remain incompletely understood. Here, we identify, with in situ hybridization, immunohistochemistry and the tissue clearing capability of iDisco, that GHRH neurons represent a unique population of arcuate nucleus neurons activated by glucose deprivation in vivo. Repeated glucose deprivation reduces GHRH neuron activation and remodels excitatory and inhibitory inputs to GHRH neurons. We show low glucose sensing is coupled to GHRH neuron depolarization, decreased ATP production and mitochondrial fusion. Repeated hypoglycemia attenuates these responses during low glucose. By maintaining mitochondrial length with the small molecule, mdivi-1, we preserved hypoglycemia sensitivity in vitro and in vivo. Our findings present possible mechanisms for the blunting of the CRR, broaden significantly our understanding of the structure of GHRH neurons and for the fist time, propose that mitochondrial dynamics play an important role in hypoglycemia unawareness. We conclude that interventions targeting mitochondrial fission in GHRH neurons may offer a new pathway to prevent hypoglycemia unawareness in diabetic patients. * *

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Automatic Dendritic Spine Quantification from Confocal Data with Neurolucida 360

Cited by 80 publications

References 46 publications

Regulation of hippocampal dendritic spines following sleep deprivation

Regulation of hippocampal dendritic spines following sleep deprivation

Apolipoprotein E regulates the maturation of injury-induced adult-born hippocampal neurons following traumatic brain injury

Repeated hypoglycemia blunts the responsiveness of glucose-inhibited GHRH neurons by remodeling neural inputs and disrupting mitochondrial structure and function

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