Time course of homeostatic structural plasticity in response to optogenetic stimulation in mouse anterior cingulate cortex DOI Creative Commons
Han Lu, Júlia V. Gallinaro, Claus Normann

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2020, Номер unknown

Опубликована: Сен. 17, 2020

Abstract Plasticity is the mechanistic basis of development, aging, learning and memory, both in healthy pathological brains. Structural plasticity rarely accounted for computational network models, due to a lack insight into underlying neuronal mechanisms processes. Little known about how rewiring networks dynamically regulated. To inform such we characterized time course neural activity, expression synaptic proteins, morphology employing an vivo optogenetic mouse model. We stimulated pyramidal neurons anterior cingulate cortex mice harvested their brains at 1.5 h, 24 48 h after stimulation. Stimulus-induced cortical hyperactivity persisted up decayed baseline indicated by c-Fos expression. The proteins VGLUT1 PSD-95, contrast, were upregulated downregulated respectively. Spine density spine head volume also increased decreased h. This specific sequence events reflects continuous joint evolution activity connectivity that characteristic model homeostatic structural plasticity. Our computer simulations thus corroborate observed empirical evidence from our animal experiments.

Язык: Английский

Differential regulations of neural activity and survival in primary cortical neurons by PFOA or PFHpA DOI Creative Commons

Moon Yi Ko,

Hee-Jin Park,

Sun‐Hwa Chon

и другие.

Chemosphere, Год журнала: 2024, Номер 352, С. 141379 - 141379

Опубликована: Фев. 3, 2024

Perfluorinated compounds (PFCs), organofluoride comprising carbon–fluorine and carbon–carbon bonds, are used as water oil repellents in textiles pharmaceutical tablets; however, they associated with potential neurotoxic effects. Moreover, the impact of PFCs on neuronal survival, activity, regulation within brain remains unclear. Additionally, mechanisms through which induce toxicity not well-understood because paucity data. This study elucidates that perfluorooctanoic acid (PFOA) perfluoroheptanoic (PFHpA) exert differential effects survival activity primary cortical neurons. Although PFOA triggers apoptosis neurons, PFHpA does exhibit this effect. Instead, modifies dendritic spine morphogenesis synapse formation cultures, additionally enhancing neural synaptic transmission. research uncovers a novel mechanism (PFHpA PFOA) cause distinct alterations shedding light molecular basis for atypical behaviors noted following PFC exposure. Understanding could guide regulatory policies usage inform clinical approaches to mitigate their effects, especially vulnerable population.

Язык: Английский

Процитировано

5
Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities DOI Open Access
Carla Liaci, Mattia Camera, Giovanni Caslini

и другие.

International Journal of Molecular Sciences, Год журнала: 2021, Номер 22(11), С. 6167 - 6167

Опубликована: Июнь 7, 2021

Intellectual disability (ID) is a pathological condition characterized by limited intellectual functioning and adaptive behaviors. It affects 1–3% of the worldwide population, no pharmacological therapies are currently available. More than 1000 genes have been found mutated in ID patients pointing out that, despite common phenotype, genetic bases highly heterogeneous apparently unrelated. Bibliomic analysis reveals that converge onto few biological modules, including cytoskeleton dynamics, whose regulation depends on Rho GTPases transduction. Genetic variants exert their effects at different levels hierarchical arrangement, starting from molecular level moving toward higher organization, i.e., cell compartment functions, circuits, cognition, behavior. Thus, alterations an impact processes such as neuronal migration, neuritogenesis, synaptic plasticity rebound overall establishment effective network consequently cognitive phenotype. Systems biology (SB) approaches more focused interconnected rather individual genes, thus encouraging design aim to correct dysregulated processes. This review summarizes current knowledge about control neurons its relevance for pathogenesis, exploiting silico modeling translating implications those findings into biomedical research.

Язык: Английский

Процитировано

21
Alterations in brain synaptic proteins and mRNAs in mood disorders: a systematic review and meta-analysis of postmortem brain studies DOI
Edison Leung,

Ethan W. Lau,

Andi Liang

и другие.

Molecular Psychiatry, Год журнала: 2022, Номер 27(3), С. 1362 - 1372

Опубликована: Янв. 13, 2022

Язык: Английский

Процитировано

16
Enhanced long-term potentiation in the anterior cingulate cortex of tree shrew DOI Creative Commons
Qian Song, Xu‐Hui Li,

Jing-Shan Lu

и другие.

Philosophical Transactions of the Royal Society B Biological Sciences, Год журнала: 2024, Номер 379(1906)

Опубликована: Июнь 10, 2024

Synaptic plasticity is a key cellular model for learning, memory and chronic pain. Most previous studies were carried out in rats mice, less known about synaptic non-human primates. In the present study, we used integrative experimental approaches to study long-term potentiation (LTP) anterior cingulate cortex (ACC) of adult tree shrews. We found that glutamate major excitatory transmitter α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid (AMPA) receptors mediate postsynaptic responses. LTP shrews was greater than mice lasted at least 5 h. N -methyl- d -aspartic acid (NMDA) receptors, Ca 2+ influx adenylyl cyclase 1 (AC1) contributed shrew LTP. Our results suggest form ACC primate-like animals. This article part discussion meeting issue 'Long-term potentiation: 50 years on'.

Язык: Английский

Процитировано

2
Time Course of Homeostatic Structural Plasticity in Response to Optogenetic Stimulation in Mouse Anterior Cingulate Cortex DOI
Han Lu, Júlia V. Gallinaro, Claus Normann

и другие.

Cerebral Cortex, Год журнала: 2021, Номер 32(8), С. 1574 - 1592

Опубликована: Июль 22, 2021

Abstract Plasticity is the mechanistic basis of development, aging, learning, and memory, both in healthy pathological brains. Structural plasticity rarely accounted for computational network models due to a lack insight into underlying neuronal mechanisms processes. Little known about how rewiring networks dynamically regulated. To inform such models, we characterized time course neural activity, expression synaptic proteins, morphology employing an vivo optogenetic mouse model. We stimulated pyramidal neurons anterior cingulate cortex mice harvested their brains at 1.5 h, 24 $48\,\mathrm{h}$ after stimulation. Stimulus-induced cortical hyperactivity persisted up h decayed baseline $24\,\mathrm{h}$ indicated by c-Fos expression. The proteins VGLUT1 PSD-95, contrast, were upregulated downregulated $48\,\mathrm{h}$, respectively. Spine density spine head volume also increased decreased $48\,\mathrm{h}$. This specific sequence events reflects continuous joint evolution activity connectivity that characteristic model homeostatic structural plasticity. Our computer simulations thus corroborate observed empirical evidence from our animal experiments.

Язык: Английский

Процитировано

12
Thalamic regulation of ocular dominance plasticity in adult visual cortex DOI Creative Commons
Yi Qin, Mehran Ahmadlou,

Samuel Suhai

и другие.

eLife, Год журнала: 2023, Номер 12

Опубликована: Июнь 23, 2023

Experience-dependent plasticity in the adult visual system is generally thought of as a cortical process. However, several recent studies have shown that perceptual learning or monocular deprivation can also induce dorsolateral geniculate nucleus (dLGN) thalamus. How thalamus and cortex interact ill-understood. To assess influence thalamic on primary (V1), we made use our previous finding during critical period ocular dominance (OD) occurs dLGN requires synaptic inhibition. Using multielectrode recordings find this true mice, absence inhibition plasticity, OD V1 absent. study silenced show period, but not adulthood, shift partially caused by feedback from V1. We conclude adulthood plays an unexpectedly dominant role experience-dependent Our findings highlight importance considering potential source events are typically processes.

Язык: Английский

Процитировано

5
Is PSD-95 entangled in the side effects of antidepressants? DOI
Katarzyna Stachowicz

Neurochemistry International, Год журнала: 2022, Номер 159, С. 105391 - 105391

Опубликована: Июль 8, 2022

Язык: Английский

Процитировано

7
miR-34a regulates silent synapse and synaptic plasticity in mature hippocampus DOI
Min Xia, Junying Wang, Fangjiao Zong

и другие.

Progress in Neurobiology, Год журнала: 2023, Номер 222, С. 102404 - 102404

Опубликована: Янв. 13, 2023

Язык: Английский

Процитировано

4
Regulatory role of the p38 MAPK/ATF2 signaling pathway in visual function and visual cortical plasticity in mice with monocular deprivation DOI

Guiqu Wang,

Yanqiong Tu,

Peixian Hou

и другие.

Neuroscience Letters, Год журнала: 2023, Номер 811, С. 137353 - 137353

Опубликована: Июнь 29, 2023

Язык: Английский

Процитировано

4
Hyperfunction of post-synaptic density protein 95 promotes seizure response in early-stage aβ pathology DOI Creative Commons
Yeeun Yook, Kwan Young Lee, Eun Young Kim

и другие.

EMBO Reports, Год журнала: 2024, Номер 25(3), С. 1233 - 1255

Опубликована: Фев. 27, 2024

Accumulation of amyloid-beta (Aβ) can lead to the formation aggregates that contribute neurodegeneration in Alzheimer's disease (AD). Despite globally reduced neural activity during AD onset, recent studies have suggested Aβ induces hyperexcitability and seizure-like early stages ultimately exacerbate cognitive decline. However, underlying mechanism is unknown. Here, we reveal an Aβ-induced elevation postsynaptic density protein 95 (PSD-95) cultured neurons vitro vivo model using APP/PS1 mice at 8 weeks age. Elevation PSD-95 occurs as a result ubiquitination caused by Akt-dependent phosphorylation E3 ubiquitin ligase murine-double-minute 2 (Mdm2). The consistent with facilitation excitatory synapses surface expression α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors induced Aβ. Inhibition corrects these synaptic defects reduces seizure mice. Our results demonstrate elevated early-stage pathology suggest could be biomarker novel therapeutic target for AD.

Язык: Английский

Процитировано

1