scholarly journals Role of drebrin A in dendritic spine plasticity and synaptic function

2009 ◽  
Vol 2 (3) ◽  
pp. 268-270 ◽  
Author(s):  
Anton Ivanov ◽  
Monique Esclapez ◽  
Lotfi Ferhat
Keyword(s):  
Dendritic Spine ◽  
Synaptic Function ◽  
Spine Plasticity

Drebrin A regulates dendritic spine plasticity and synaptic function in mature cultured hippocampal neurons

2009 ◽  
Vol 122 (4) ◽  
pp. 524-534 ◽  
Author(s):  
A. Ivanov ◽  
M. Esclapez ◽  
C. Pellegrino ◽  
T. Shirao ◽  
L. Ferhat
Keyword(s):  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Synaptic Function ◽  
Spine Plasticity ◽  
Cultured Hippocampal Neurons

Ibotenic acid induced lesions impair the modulation of dendritic spine plasticity in the prefrontal cortex and amygdala, a phenomenon that underlies working memory and social behavior

2021 ◽  
Vol 896 ◽  
pp. 173883
Author(s):  
Néstor I. Martínez-Torres ◽  
Nallely Vázquez-Hernández ◽  
Fabiola L. Martín-Amaya-Barajas ◽  
Mario Flores-Soto ◽  
Ignacio González-Burgos
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Social Behavior ◽  
Dendritic Spine ◽  
Ibotenic Acid ◽  
Spine Plasticity

scholarly journals Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson’s Disease

2019 ◽  
Vol 20 (14) ◽  
pp. 3407 ◽  
Author(s):  
Paola Imbriani ◽  
Annalisa Tassone ◽  
Maria Meringolo ◽  
Giulia Ponterio ◽  
Graziella Madeo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Caspase 3 ◽  
Cysteine Proteases ◽  
Synaptic Function ◽  
Adult Brain ◽  
Striatal Slices

Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.

Sensory Transmission is Bi-directionally Modulated by Astrocytic Ca2+ in Barrel Cortex of Behaving Mice

2021 ◽  
Author(s):  
Simeng Gu ◽  
Wei Wang ◽  
Kuan Zhang ◽  
Rou Feng ◽  
Naling Li ◽  
...  
Keyword(s):  
Sensory Input ◽  
Barrel Cortex ◽  
Synaptic Function ◽  
Metabolic Clearance ◽  
Sleep State ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Sensory Transmission

Abstract Different effects of astrocyte during sleep and awake have been extensively studied, especially for metabolic clearance by the glymphatic system, which works during sleep and stops working during waking states. However, how astrocytes contribute to modulation of sensory transmission during sleep and awake animals remain largely unknown. Recent advances in genetically encoded Ca2+ indicators have provided a wealth of information on astrocytic Ca2+, especially in their fine perisynaptic processes, where astrocytic Ca2+ most likely affects the synaptic function. Here we use two-photon microscopy to image astrocytic Ca2+ signaling in freely moving mice trained to run on a wheel in combination with in vivo whole-cell recordings to evaluate the role of astrocytic Ca2+ signaling in different behavior states. We found that there are two kinds of astrocytic Ca2+ signaling: a small long-lasting Ca2+ increase during sleep state and a sharp widespread but short-long-lasting Ca2+ spike when the animal was awake (fluorescence increases were 23.2 ± 14.4% for whisker stimulation at sleep state, compared with 73.3 ± 11.7% for at awake state, paired t-test, p < 0.01). The small Ca2+ transients decreased extracellular K+, hyperpolarized the neurons, and suppressed sensory transmission; while the large Ca2+ wave enhanced sensory input, contributing to reliable sensory transmission in aroused states. Locus coeruleus activation works as a switch between these two kinds of astrocytic Ca2+ elevation. Thus, we show that cortical astrocytes play an important role in processing of sensory input. These two types of events appear to have different pharmacological sources and may play a different role in facilitating the efficacy of sensory transmission.

scholarly journals Intracellular Ca2+ Release and Synaptic Plasticity: A Tale of Many Stores

2018 ◽  
Vol 25 (3) ◽  
pp. 208-226 ◽  
Author(s):  
Zahid Padamsey ◽  
William J. Foster ◽  
Nigel J. Emptage
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Synaptic Function ◽  
Intracellular Organelles ◽  
Short And Long Term ◽  
Central Synapses ◽  
Neural Signaling ◽  
Temporal Extent

Ca2+ is an essential trigger for most forms of synaptic plasticity. Ca2+ signaling occurs not only by Ca2+ entry via plasma membrane channels but also via Ca2+ signals generated by intracellular organelles. These organelles, by dynamically regulating the spatial and temporal extent of Ca2+ elevations within neurons, play a pivotal role in determining the downstream consequences of neural signaling on synaptic function. Here, we review the role of three major intracellular stores: the endoplasmic reticulum, mitochondria, and acidic Ca2+ stores, such as lysosomes, in neuronal Ca2+ signaling and plasticity. We provide a comprehensive account of how Ca2+ release from these stores regulates short- and long-term plasticity at the pre- and postsynaptic terminals of central synapses.

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