scholarly journals Hyperforin modulates dendritic spine morphology in hippocampal pyramidal neurons by activating Ca2+-permeable TRPC6 channels

Hippocampus ◽  
2012 ◽  
Vol 23 (1) ◽  
pp. 40-52 ◽  
Author(s):  
Kristina Leuner ◽  
Wei Li ◽  
Michelle D. Amaral ◽  
Stephanie Rudolph ◽  
Gaston Calfa ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Morphology ◽  
Hippocampal Pyramidal Neurons ◽  
Dendritic Spine Morphology

scholarly journals Impact of JNK and Its Substrates on Dendritic Spine Morphology

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 440 ◽  
Author(s):  
Emilia Komulainen ◽  
Artemis Varidaki ◽  
Natalia Kulesskaya ◽  
Hasan Mohammad ◽  
Christel Sourander ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Lucifer Yellow ◽  
Dendrite Morphology ◽  
Spine Morphology ◽  
Kinase Substrate ◽  
Basal Dendrites ◽  
Dendritic Spine Morphology ◽  
Mushroom Spines

The protein kinase JNK1 exhibits high activity in the developing brain, where it regulates dendrite morphology through the phosphorylation of cytoskeletal regulatory proteins. JNK1 also phosphorylates dendritic spine proteins, and Jnk1-/- mice display a long-term depression deficit. Whether JNK1 or other JNKs regulate spine morphology is thus of interest. Here, we characterize dendritic spine morphology in hippocampus of mice lacking Jnk1-/- using Lucifer yellow labelling. We find that mushroom spines decrease and thin spines increase in apical dendrites of CA3 pyramidal neurons with no spine changes in basal dendrites or in CA1. Consistent with this spine deficit, Jnk1-/- mice display impaired acquisition learning in the Morris water maze. In hippocampal cultures, we show that cytosolic but not nuclear JNK, regulates spine morphology and expression of phosphomimicry variants of JNK substrates doublecortin (DCX) or myristoylated alanine-rich C kinase substrate-like protein-1 (MARCKSL1), rescue mushroom, thin, and stubby spines differentially. These data suggest that physiologically active JNK controls the equilibrium between mushroom, thin, and stubby spines via phosphorylation of distinct substrates.

scholarly journals Conditional deletion of ROCK2 induces anxiety-like behaviors and alters dendritic spine density and morphology on CA1 pyramidal neurons

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Audrey J. Weber ◽  
Ashley B. Adamson ◽  
Kelsey M. Greathouse ◽  
Julia P. Andrade ◽  
Cameron D. Freeman ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Basolateral Amygdala ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Spine Density ◽  
Control Of Gene Expression ◽  
Spine Morphology ◽  
Dendritic Spine Morphology ◽  
Morphometry Analysis ◽  
Apical Dendrites

AbstractRho-associated kinase isoform 2 (ROCK2) is an attractive drug target for several neurologic disorders. A critical barrier to ROCK2-based research and therapeutics is the lack of a mouse model that enables investigation of ROCK2 with spatial and temporal control of gene expression. To overcome this, we generated ROCK2fl/fl mice. Mice expressing Cre recombinase in forebrain excitatory neurons (CaMKII-Cre) were crossed with ROCK2fl/fl mice (Cre/ROCK2fl/fl), and the contribution of ROCK2 in behavior as well as dendritic spine morphology in the hippocampus, medial prefrontal cortex (mPFC), and basolateral amygdala (BLA) was examined. Cre/ROCK2fl/fl mice spent reduced time in the open arms of the elevated plus maze and increased time in the dark of the light–dark box test compared to littermate controls. These results indicated that Cre/ROCK2fl/fl mice exhibited anxiety-like behaviors. To examine dendritic spine morphology, individual pyramidal neurons in CA1 hippocampus, mPFC, and the BLA were targeted for iontophoretic microinjection of fluorescent dye, followed by high-resolution confocal microscopy and neuronal 3D reconstructions for morphometry analysis. In dorsal CA1, Cre/ROCK2fl/fl mice displayed significantly increased thin spine density on basal dendrites and reduced mean spine head volume across all spine types on apical dendrites. In ventral CA1, Cre/ROCK2fl/fl mice exhibited significantly increased spine length on apical dendrites. Spine density and morphology were comparable in the mPFC and BLA between both genotypes. These findings suggest that neuronal ROCK2 mediates spine density and morphology in a compartmentalized manner among CA1 pyramidal cells, and that in the absence of ROCK2 these mechanisms may contribute to anxiety-like behaviors.

scholarly journals Splice variants of the CaV1.3 L-type calcium channel regulate dendritic spine morphology

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Ruslan Stanika ◽  
Marta Campiglio ◽  
Alexandra Pinggera ◽  
Amy Lee ◽  
Jörg Striessnig ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Dendritic Spine ◽  
Splice Variants ◽  
Spine Morphology ◽  
Dendritic Spine Morphology

SIRT1 Regulates Tau Expression and Tau Synaptic Pathology

2021 ◽  
pp. 1-10
Author(s):  
Xiaomin Yin ◽  
Zheng Zhou ◽  
Yanyan Qiu ◽  
Xing Fan ◽  
Chenhao Zhao ◽  
...  
Keyword(s):  
Neurofibrillary Tangles ◽  
Dendritic Spine ◽  
Amyloid Plaques ◽  
Transcriptional Level ◽  
Spine Morphology ◽  
Protein Levels ◽  
Dendritic Spine Morphology ◽  
Synaptic Pathology ◽  
Factor C ◽  
Tau Expression

Background: Amyloid plaques and neurofibrillary tangles are two pathological hallmarks of Alzheimer’s disease (AD). However, synaptic deficits occur much earlier and correlate stronger with cognitive decline than amyloid plaques and neurofibrillary tangles. Mislocalization of tau is an early hallmark of neurodegeneration and precedes aggregations. Sirtuin type 1 (SIRT1) is a deacetylase which acts on proteins including transcriptional factors and associates closely with AD. Objective: The present study investigated the association between SIRT1 and tau expression in cells and in mice brains. Methods: Western blot was performed to detected tau, SIRT1, C/EBPα, and GAPDH protein levels. Immunological fluorescence assay was used to assess tau localization in primary cortical neuronal cells. Golgi staining was performed to evaluated dendritic spine morphology in mice brains. Results: In the present study, we found that SIRT1 negatively regulates expression of tau at the transcriptional level through transcriptional factor C/EBPα. Inhibition of the activity of SIRT1 limits the distribution of tau to the neurites. In the meantime, the alteration of dendritic spine morphology is also observed in the brains of SIRT1+/– mice. Conclusion: SIRT1 may be a potential drug target for early intervention in AD.

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