Dendritic spine abnormalities in the occipital cortex of C57BL/6Fmr1 knockout mice

2005 ◽  
Vol 136B (1) ◽  
pp. 98-102 ◽  
Author(s):  
Brandon C. McKinney ◽  
Aaron W. Grossman ◽  
Nicholas M. Elisseou ◽  
William T. Greenough
Keyword(s):  
Dendritic Spine ◽  
Knockout Mice ◽  
Occipital Cortex ◽  
Spine Abnormalities

Subregion-specific dendritic spine abnormalities in the hippocampus of Fmr1 KO mice

2011 ◽  
Vol 95 (4) ◽  
pp. 467-472 ◽  
Author(s):  
Josien Levenga ◽  
Femke M.S. de Vrij ◽  
Ronald A.M. Buijsen ◽  
Tracy Li ◽  
Ingeborg M. Nieuwenhuizen ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Spine Abnormalities

scholarly journals Decreased dendritic spine density and abnormal spine morphology in Fyn knockout mice

2011 ◽  
Vol 1415 ◽  
pp. 96-102 ◽  
Author(s):  
Lenard W. Babus ◽  
Elizabeth M. Little ◽  
Kathleen E. Keenoy ◽  
S. Sakura Minami ◽  
Eric Chen ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Knockout Mice ◽  
Spine Density ◽  
Spine Morphology ◽  
Dendritic Spine Density

Development and Regulation of Dendritic Spine Synapses

Physiology ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Barbara Calabrese ◽  
Margaret S. Wilson ◽  
Shelley Halpain
Keyword(s):  
Synaptic Transmission ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Excitatory Synapses ◽  
Dense Array ◽  
Complex Dynamic ◽  
Neuronal Dendrites ◽  
Spine Abnormalities ◽  
Dynamic Structures ◽  
The Brain

Dendritic spines are small protrusions from neuronal dendrites that form the postsynaptic component of most excitatory synapses in the brain. They play critical roles in synaptic transmission and plasticity. Recent advances in imaging and molecular technologies reveal that spines are complex, dynamic structures that contain a dense array of cytoskeletal, transmembrane, and scaffolding molecules. Several neurological and psychiatric disorders exhibit dendritic spine abnormalities.

scholarly journals Dendritic spine morphology and memory formation depend on postsynaptic Caskin proteins

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Norbert Bencsik ◽  
Szilvia Pusztai ◽  
Sándor Borbély ◽  
Anna Fekete ◽  
Metta Dülk ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Knockout Mice ◽  
Hippocampal Neurons ◽  
Pain Perception ◽  
Hippocampal Slices ◽  
Scaffold Proteins ◽  
Double Knockout ◽  
Learning Abilities ◽  
Spine Morphology

AbstractCASK-interactive proteins, Caskin1 and Caskin2, are multidomain neuronal scaffold proteins. Recent data from Caskin1 knockout animals indicated only a mild role of Caskin1 in anxiety and pain perception. In this work, we show that deletion of both Caskins leads to severe deficits in novelty recognition and spatial memory. Ultrastructural analyses revealed a reduction in synaptic profiles and dendritic spine areas of CA1 hippocampal pyramidal neurons of double knockout mice. Loss of Caskin proteins impaired LTP induction in hippocampal slices, while miniature EPSCs in dissociated hippocampal cultures appeared to be unaffected. In cultured Caskin knockout hippocampal neurons, overexpressed Caskin1 was enriched in dendritic spine heads and increased the amount of mushroom-shaped dendritic spines. Chemically induced LTP (cLTP) mediated enlargement of spine heads was augmented in the knockout mice and was not influenced by Caskin1. Immunocytochemistry and immunoprecipitation confirmed that Shank2, a master scaffold of the postsynaptic density, and Caskin1 co-localized within the same complex. Phosphorylation of AMPA receptors was specifically altered by Caskin deficiency and was not elevated by cLTP treatment further. Taken together, our results prove a previously unnoticed postsynaptic role of Caskin scaffold proteins and indicate that Caskins influence learning abilities via regulating spine morphology and AMPA receptor localisation.

scholarly journals Early Postnatal Plasticity in Neocortex of Fmr1 Knockout Mice

2006 ◽  
Vol 96 (4) ◽  
pp. 1734-1745 ◽  
Author(s):  
Niraj S. Desai ◽  
Tanya M. Casimiro ◽  
Stephen M. Gruber ◽  
Peter W. Vanderklish
Keyword(s):  
Knockout Mice ◽  
Developmental Plasticity ◽  
Fragile X ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Spike Timing ◽  
Term Potentiation ◽  
Spine Abnormalities ◽  
Intrinsic Plasticity

Fragile X syndrome is produced by a defect in a single X-linked gene, called Fmr1, and is characterized by abnormal dendritic spine morphologies with spines that are longer and thinner in neocortex than those from age-matched controls. Studies using Fmr1 knockout mice indicate that spine abnormalities are especially pronounced in the first month of life, suggesting that altered developmental plasticity underlies some of the behavioral phenotypes associated with the syndrome. To address this issue, we used intracellular recordings in neocortical slices from early postnatal mice to examine the effects of Fmr1 disruption on two forms of plasticity active during development. One of these, long-term potentiation of intrinsic excitability, is intrinsic in expression and requires mGluR5 activation. The other, spike timing-dependent plasticity, is synaptic in expression and requires N-methyl-d-aspartate receptor activation. While intrinsic plasticity was normal in the knockout mice, synaptic plasticity was altered in an unusual and striking way: long-term depression was robust but long-term potentiation was entirely absent. These findings underscore the ideas that Fmr1 has highly selective effects on plasticity and that abnormal postnatal development is an important component of the disorder.

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