Do thin spines learn to be mushroom spines that remember?

Bourne, Jennifer N.; Harris, Kristen M.

doi:10.1016/j.conb.2007.04.009

Cited by 760 publications

(730 citation statements)

References 58 publications

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“…This suggests that the learning capabilities of SAMP8 decrease, since thin spines have been related with information acquisition (learning) [108][109][110]. This is in agreement with the finding that SAMP8 was inefficient at resolving the object recognition test at 9 months of age.…”

Section: Behavioral Characteristicssupporting

confidence: 80%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer's disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.

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Section: Behavioral Characteristicssupporting

confidence: 80%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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“…Thin dendritic spines are immature synaptic structures that are highly plastic in nature, and possess smaller spine heads, consistent with our finding of an overall decrease in the average spine head volume. These spines readily stabilize or retract in response to increased or weakened synaptic input (Bourne and Harris, 2007), making them prime candidates for synaptic reorganization. Interestingly, immature synaptic structures are known to predominately express the GluN2B receptor (Sheng et al, 1994), and ketamine, a potent NMDA receptor antagonist, along with GluN2B-specific antagonists have rapid antidepressant effects in multiple models of depression (Autry et al, 2011;Li et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Effects of Inhibitor of κB Kinase Activity in the Nucleus Accumbens on Emotional Behavior

Christoffel

Golden

Heshmati

et al. 2012

Neuropsychopharmacol

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Inhibitor of kB kinase (IkK) has historically been studied in the context of immune response and inflammation, but recent evidence demonstrates that IkK activity is necessary and sufficient for regulation of neuronal function. Chronic social defeat stress of mice increases IkK activity in the nucleus accumbens (NAc) and this increase is strongly correlated to depression-like behaviors. Inhibition of IkK signaling results in a reversal of chronic social defeat stress-induced social avoidance behavior. Here, we more completely define the role of IkK in anxiety and depressive-like behaviors. Mice underwent stereotaxic microinjection of a herpes simplex virus expressing either green fluorescent protein, a constitutively active form of IkK (IkKca), or a dominant negative form of IkK into the NAc. Of all three experimental groups, only mice expressing IkKca show a behavioral phenotype. Expression of IkKca results in a decrease in the time spent in the nonperiphery zones of an open field arena and increased time spent immobile during a forced swim test. No baseline differences in sucrose preference were observed, but following the acute swim stress we noted a marked reduction in sucrose preference. To determine whether IkK activity alters responses to other acute stressors, we examined behavior and spine morphology in mice undergoing an acute social defeat stress. We found that IkKca enhanced social avoidance behavior and promoted thin spine formation. These data show that IkK in NAc is a critical regulator of both depressive-and anxiety-like states and may do so by promoting the formation of immature excitatory synapses.

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“…As excision of the Stim2 gene occurs in adult Stim2 cKO mice after spinogenesis, this deficit in mushroom spines most likely reflects a failure in the maintenance of mature spines rather than a developmental defect. It has been proposed that stable mushroom 9 spines store information over long-period of times 33 . Reduced number of mushroom spines in Stim2-depleted pyramidal cells is therefore consistent with impaired plasticity and information processing in these mice.…”

Section: Stim2 Regulates Dendritic Spine Shape and Densitymentioning

confidence: 99%

STIM2 regulates AMPA receptor trafficking and plasticity at hippocampal synapses

Yap

Shetty

García-Alvarez

et al. 2017

Neurobiology of Learning and Memory

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STIM2 is an integral membrane protein of the endoplasmic reticulum (ER) that regulates the activity of plasma membrane (PM) channels at ER-PM contact sites. Recent studies show that STIM2 promotes spine maturation and surface expression of the AMPA receptor (AMPAR) subunit GluA1, hinting to a probable role in synaptic plasticity. Here, we used a Stim2 cKO mouse line to explore the function of STIM2 in early forms of Long-Term Potentiation (E-LTP) and Depression (E-LTD), two widely-studied models of synaptic plasticity implicated in information storage. We found that STIM2 is required for the stable expression of both E-LTP and E-LTD at CA3-CA1 hippocampal synapses. Altered plasticity in Stim2 cKO mice is associated with subtle alterations in the shape and density of dendritic spines in CA1 neurons.Further, surface delivery of GluA1 in response to LTP-inducing chemical manipulations was markedly reduced in excitatory neurons derived from Stim2 cKO mice. In addition, NMDAinduced GluA1 endocytosis, which underlies LTD, was impaired in Stim2 cKO neurons. We conclude that STIM2 facilitates synaptic delivery and removal of AMPARs and regulates activity-dependent changes in synaptic strength through a unique mode of communication between the ER and the synapse.

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Do thin spines learn to be mushroom spines that remember?

Cited by 760 publications

References 58 publications

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Effects of Inhibitor of κB Kinase Activity in the Nucleus Accumbens on Emotional Behavior

STIM2 regulates AMPA receptor trafficking and plasticity at hippocampal synapses

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