Cold‐induced exodus of postsynaptic proteins from dendritic spines

Cheng, Hui-Hsuan; Huang, Zhi; Lin, Wei‐Hsiang; Chow, Wei-Yuan; Chang, Y. C.

doi:10.1002/jnr.21852

Cited by 16 publications

(7 citation statements)

References 48 publications

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“…The apparent increase in transmitter release / quantal content in the warm-acclimatized group, without a concomitant increase in EJP amplitude, could be due to reduced sensitivity of postsynaptic receptors to the transmitter [50]. This is consistent with the partial decline in post-synaptic responsiveness to glutamate in the warm-acclimatized group (Figure 4B) and a significant reduction in the amplitude of single, evoked quantal currents (Figure S2).…”

Section: Discussionsupporting

confidence: 77%

Cholesterol-Independent Effects of Methyl-β-Cyclodextrin on Chemical Synapses

et al. 2012

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The cholesterol chelating agent, methyl-β-cyclodextrin (MβCD), alters synaptic function in many systems. At crayfish neuromuscular junctions, MβCD is reported to reduce excitatory junctional potentials (EJPs) by impairing impulse propagation to synaptic terminals, and to have no postsynaptic effects. We examined the degree to which physiological effects of MβCD correlate with its ability to reduce cholesterol, and used thermal acclimatization as an alternative method to modify cholesterol levels. MβCD impaired impulse propagation and decreased EJP amplitude by 40% (P<0.05) in preparations from crayfish acclimatized to 14°C but not from those acclimatized to 21°C. The reduction in EJP amplitude in the cold-acclimatized group was associated with a 49% reduction in quantal content (P<0.05). MβCD had no effect on input resistance in muscle fibers but decreased sensitivity to the neurotransmitter L-glutamate in both warm- and cold-acclimatized groups. This effect was less pronounced and reversible in the warm-acclimatized group (90% reduction in cold, P<0.05; 50% reduction in warm, P<0.05). MβCD reduced cholesterol in isolated nerve and muscle from cold- and warm-acclimatized groups by comparable amounts (nerve: 29% cold, 25% warm; muscle: 20% cold, 18% warm; P<0.05). This effect was reversed by cholesterol loading, but only in the warm-acclimatized group. Thus, effects of MβCD on glutamate-sensitivity correlated with its ability to reduce cholesterol, but effects on impulse propagation and resulting EJP amplitude did not. Our results indicate that MβCD can affect both presynaptic and postsynaptic properties, and that some effects of MβCD are unrelated to cholesterol chelation.

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Section: Discussionsupporting

confidence: 77%

Cholesterol-Independent Effects of Methyl-β-Cyclodextrin on Chemical Synapses

et al. 2012

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“…Primary hippocampal neurons were dissociated from the rat fetuses at the 18th embryonic day according to the procedures previously described [ 72 , 73 ]. Inhibition of the expression of the tau protein was conducted in neuronal cells (N2A and hippocampal neurons).…”

Section: Methodsmentioning

confidence: 99%

Potential Natural Products for Alzheimer’s Disease: Targeted Search Using the Internal Ribosome Entry Site of Tau and Amyloid-β Precursor Protein

Tasi

Chin

Chen

et al. 2015

IJMS

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Overexpression of the amyloid precursor protein (APP) and the hyperphosphorylation of the tau protein are vital in the understanding of the cause of Alzheimer’s disease (AD). As a consequence, regulation of the expression of both APP and tau proteins is one important approach in combating AD. The APP and tau proteins can be targeted at the levels of transcription, translation and protein structural integrity. This paper reports the utilization of a bi-cistronic vector containing either APP or tau internal ribosome entry site (IRES) elements flanked by β-galactosidase gene (cap-dependent) and secreted alkaline phosphatase (SEAP) (cap-independent) to discern the mechanism of action of memantine, an N-methyl-d-aspartate (NMDA) receptor antagonist. Results indicate that memantine could reduce the activity of both the APP and tau IRES at a concentration of ~10 μM (monitored by SEAP activity) without interfering with the cap-dependent translation as monitored by the β-galactosidase assay. Western blot analysis of the tau protein in neuroblastoma (N2A) and rat hippocampal cells confirmed the halting of the expression of the tau proteins. We also employed this approach to identify a preparation named NB34, extracts of Boussingaultia baselloides (madeira-vine) fermented with Lactobacillus spp., which can function similarly to memantine in both IRES of APP and Tau. The water maze test demonstrated that NB34 could improve the spatial memory of a high fat diet induced neurodegeneration in apolipoprotein E-knockout (ApoE−/−) mice. These results revealed that the bi-cistronic vector provided a simple, and effective platform in screening and establishing the mechanistic action of potential compounds for the treatment and management of AD.

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“…(9,115,192,204). Some of these changes of spine regression and translocation of postsynaptic proteins away from the synapse can be mimicked in vitro by cooling of brain slices (30,102,166). Still, the in vivo effects of hypothermia on spines in the hippocampus are rather small (154) or even absent in the neocortex (218).…”

Section: Neuronal Plasticity During Hibernationmentioning

confidence: 99%

Neuronal plasticity in hibernation and the proposed role of the microtubule-associated protein tau as a “master switch” regulating synaptic gain in neuronal networks

Arendt

Bullmann

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Arendt T, Bullmann T. Neuronal plasticity in hibernation and the proposed role of the microtubule-associated protein tau as a "master switch" regulating synaptic gain in neuronal networks. Am J Physiol Regul Integr Comp Physiol 305: R478 -R489, 2013. First published July 13, 2013 doi:10.1152/ajpregu.00117.2013.-The present paper provides an overview of adaptive changes in brain structure and learning abilities during hibernation as a behavioral strategy used by several mammalian species to minimize energy expenditure under current or anticipated inhospitable environmental conditions. One cellular mechanism that contributes to the regulated suppression of metabolism and thermogenesis during hibernation is reversible phosphorylation of enzymes and proteins, which limits rates of flux through metabolic pathways. Reversible phosphorylation during hibernation also affects synaptic membrane proteins, a process known to be involved in synaptic plasticity. This mechanism of reversible protein phosphorylation also affects the microtubule-associated protein tau, thereby generating a condition that in the adult human brain is associated with aggregation of tau protein to paired helical filaments (PHFs), as observed in Alzheimer's disease. Here, we put forward the concept that phosphorylation of tau is a neuroprotective mechanism to escape NMDA-mediated hyperexcitability of neurons that would otherwise occur during slow gradual cooling of the brain. Phosphorylation of tau and its subsequent targeting to subsynaptic sites might, thus, work as a kind of "master switch," regulating NMDA receptor-mediated synaptic gain in a wide array of neuronal networks, thereby enabling entry into torpor. If this condition lasts too long, however, it may eventually turn into a pathological trigger, driving a cascade of events leading to neurodegeneration, as in Alzheimer's disease or other "tauopathies".Alzheimer's disease; neurodegeneration; neuroprotection; neuronal plasticity; protein phosphorylation; tauopathies Seasonal Brain Plasticity Might Be a Widespread PhenomenonANIMALS LIVING IN ENVIRONMENTS with daily or seasonal rhythms have developed different strategies to coordinate endogenous processes with ambient conditions. To optimize their energy balance under conditions of restricted availability of food and increased costs for temperature regulation, animals can either reduce the expense for foraging or the need of foraging (96). The expense for foraging can be reduced by food storing or escaping a cold climate by migration. Alternatively, hibernation is a powerful strategy to reduce the metabolic costs of daily activity. All of these aforementioned strategies to optimize energy expenditure are associated with plastic adaptive changes both at the level of behavior and brain structure.The seasonal modulation of food-storing behavior (33,177,178,182) or migration (17) in birds has been shown to require special spatial learning abilities, which are paralleled by seasonal changes in neuronal structure. These cyclic changes in size and mo...

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Cold‐induced exodus of postsynaptic proteins from dendritic spines

Cited by 16 publications

References 48 publications

Cholesterol-Independent Effects of Methyl-β-Cyclodextrin on Chemical Synapses

Cholesterol-Independent Effects of Methyl-β-Cyclodextrin on Chemical Synapses

Potential Natural Products for Alzheimer’s Disease: Targeted Search Using the Internal Ribosome Entry Site of Tau and Amyloid-β Precursor Protein

Neuronal plasticity in hibernation and the proposed role of the microtubule-associated protein tau as a “master switch” regulating synaptic gain in neuronal networks

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