Reliable and durable Golgi staining of brain tissue from human autopsies and experimental animals

Rosoklija, Gorazd; Petruševski, Vladimir M.; Stankov, Aleksandar; Dika, Ani; Jakovski, Zlatko; Pavlovski, Goran; Davcheva, Natasha; Lipkin, R.; Schnieder, Tatiana; Scobie, Kimberley; Duma, A.; Dwork, Andrew J.

doi:10.1016/j.jneumeth.2014.04.006

Cited by 21 publications

(14 citation statements)

References 15 publications

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“…The success of Golgi‐Kopsch staining in the current set of postmortem human tissue was consistent with previous studies (Jacobs et al, ; Rosoklija et al, ), allowing quantitative data collection from 27 (13 TD and 14 ASD) of the 32 brains processed, yielding data from a total of 270 traced neurons (Figure ). Example photomicrographs of lateral nucleus amygdala neurons from typically developing and ASD individuals during childhood and adulthood are depicted in Figure .…”

Section: Resultsmentioning

confidence: 99%

Protracted dendritic growth in the typically developing human amygdala and increased spine density in young ASD brains

Weir

Bauman

Jacobs

et al. 2017

J of Comparative Neurology

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The amygdala is a medial temporal lobe structure implicated in social and emotional regulation. In typical development (TD), the amygdala continues to increase volumetrically throughout childhood and into adulthood, while other brain structures are stable or decreasing in volume. In autism spectrum disorder (ASD), the amygdala undergoes rapid early growth, making it volumetrically larger in children with ASD compared to TD children. Here we explore: (a) if dendritic arborization in the amygdala follows the pattern of protracted growth in TD and early overgrowth in ASD and (b), if spine density in the amygdala in ASD cases differs from TD from youth to adulthood. The amygdala from 32 postmortem human brains (7–46 years of age) were stained using a Golgi-Kopsch impregnation. Ten principal neurons per case were selected in the lateral nucleus and traced using Neurolucida software in their entirety. We found that both ASD and TD individuals show a similar pattern of increasing dendritic length with age well into adulthood. However, spine density is (a) greater in young ASD cases compared to age-matched TD controls (<18 years old) and (b) decreases in the amygdala as people with ASD age into adulthood, a phenomenon not found in TD. Therefore, by adulthood, there is no observable difference in spine density in the amygdala between ASD and TD age-matched adults (≥18 years old). Our findings highlight the unique growth trajectory of the amygdala and suggest that spine density may contribute to aberrant development and function of the amygdala in children with ASD.

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Section: Resultsmentioning

confidence: 99%

Protracted dendritic growth in the typically developing human amygdala and increased spine density in young ASD brains

Weir

Bauman

Jacobs

et al. 2017

J of Comparative Neurology

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“…injection, mice were sacrificed with a lethal dose of anaesthetic (Zoletil/Rompun 800 and 100 mg/kg, respectively) and perfused transcardially with 0.9% saline solution. Brains were dissected and immediately immersed in a Golgi-Cox solution (1% K 2 Cr 2 O 7 , 1% HgCl 2 and 0.8% K 2 CrO 4 ) at RT for 6 days, according to a previously described protocol ( Gibb and Kolb, 1998 ; Rosoklija et al , 2014 ). On the seventh day, brains were transferred in a 30% sucrose solution for cryoprotection and then sectioned with a vibratome.…”

Section: Methodsmentioning

confidence: 99%

Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse Alzheimer’s disease models

Corsetti

Borreca

Latina

et al. 2020

Brain Communications

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Clinical and neuropathological studies have shown that tau pathology better correlates with the severity of dementia than amyloid plaque burden, making tau an attractive target for the cure of Alzheimer’s disease. We have explored whether passive immunization with the 12A12 monoclonal antibody (26–36aa of tau protein) could improve the Alzheimer’s disease phenotype of two well-established mouse models, Tg2576 and 3xTg mice. 12A12 is a cleavage-specific monoclonal antibody which selectively binds the pathologically relevant neurotoxic NH226-230 fragment (i.e. NH2htau) of tau protein without cross-reacting with its full-length physiological form(s). We found out that intravenous administration of 12A12 monoclonal antibody into symptomatic (6 months old) animals: (i) reaches the hippocampus in its biologically active (antigen-binding competent) form and successfully neutralizes its target; (ii) reduces both pathological tau and amyloid precursor protein/amyloidβ metabolisms involved in early disease-associated synaptic deterioration; (iii) improves episodic-like type of learning/memory skills in hippocampal-based novel object recognition and object place recognition behavioural tasks; (iv) restores the specific up-regulation of the activity-regulated cytoskeleton-associated protein involved in consolidation of experience-dependent synaptic plasticity; (v) relieves the loss of dendritic spine connectivity in pyramidal hippocampal CA1 neurons; (vi) rescues the Alzheimer’s disease-related electrophysiological deficits in hippocampal long-term potentiation at the CA3-CA1 synapses; and (vii) mitigates the neuroinflammatory response (reactive gliosis). These findings indicate that the 20–22 kDa NH2-terminal tau fragment is crucial target for Alzheimer’s disease therapy and prospect immunotherapy with 12A12 monoclonal antibody as safe (normal tau-preserving), beneficial approach in contrasting the early Amyloidβ-dependent and independent neuropathological and cognitive alterations in affected subjects.

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“…Techniques commonly used in humans to study brain organization such as EEG, MEG, and MRI lack cellular resolution. Molecular and histological approaches using postmortem human brain material have limitations to unravel extensive subcellular architecture, since typically, only partial cellular morphologies can be resolved and quantitative analysis is performed on subcompartments of the apical/basal dendritic tree ( Braak 1980 ; Ong and Garey 1990 ; Elston et al 2001 ; Jacobs et al 2001 ; Anderson et al 2009 ; Petanjek et al 2011 ; Rosoklija et al 2014 ). Additionally, postmortem delays to brain tissue fixation may effect morphology of fine cellular structures ( de Ruiter and Uylings 1987 ; Swaab and Uylings 1988 ; Oberheim et al 2009 ).…”

Section: Introductionmentioning

confidence: 99%

Dendritic and Axonal Architecture of Individual Pyramidal Neurons across Layers of Adult Human Neocortex

et al. 2015

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The size and shape of dendrites and axons are strong determinants of neuronal information processing. Our knowledge on neuronal structure and function is primarily based on brains of laboratory animals. Whether it translates to human is not known since quantitative data on “full” human neuronal morphologies are lacking. Here, we obtained human brain tissue during resection surgery and reconstructed basal and apical dendrites and axons of individual neurons across all cortical layers in temporal cortex (Brodmann area 21). Importantly, morphologies did not correlate to etiology, disease severity, or disease duration. Next, we show that human L(ayer) 2 and L3 pyramidal neurons have 3-fold larger dendritic length and increased branch complexity with longer segments compared with temporal cortex neurons from macaque and mouse. Unsupervised cluster analysis classified 88% of human L2 and L3 neurons into human-specific clusters distinct from mouse and macaque neurons. Computational modeling of passive electrical properties to assess the functional impact of large dendrites indicates stronger signal attenuation of electrical inputs compared with mouse. We thus provide a quantitative analysis of “full” human neuron morphologies and present direct evidence that human neurons are not “scaled-up” versions of rodent or macaque neurons, but have unique structural and functional properties.

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Reliable and durable Golgi staining of brain tissue from human autopsies and experimental animals

Cited by 21 publications

References 15 publications

Protracted dendritic growth in the typically developing human amygdala and increased spine density in young ASD brains

Protracted dendritic growth in the typically developing human amygdala and increased spine density in young ASD brains

Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse Alzheimer’s disease models

Dendritic and Axonal Architecture of Individual Pyramidal Neurons across Layers of Adult Human Neocortex

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