scholarly journals Role of dopaminergic and GABAergic mechanisms in discrete brain areas in phencyclidine-induced locomotor stimulation and turning behavior.

1986 ◽  
Vol 9 (12) ◽  
pp. 975-986 ◽  
Author(s):  
KAZUMASA YAMAGUCHI ◽  
TOSHITAKA NABESHIMA ◽  
TSUTOMU KAMEYAMA
Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3578
Author(s):  
Federica Mastroiacovo ◽  
Francesca Biagioni ◽  
Paola Lenzi ◽  
Larisa Ryskalin ◽  
Stefano Puglisi-Allegra ◽  
...  

The heat shock protein (HSP) 70 is considered the main hallmark in preclinical studies to stain the peri-infarct region defined area penumbra in preclinical models of brain ischemia. This protein is also considered as a potential disease modifier, which may improve the outcome of ischemic damage. In fact, the molecule HSP70 acts as a chaperonine being able to impact at several level the homeostasis of neurons. Despite being used routinely to stain area penumbra in light microscopy, the subcellular placement of this protein within area penumbra neurons, to our knowledge, remains undefined. This is key mostly when considering studies aimed at deciphering the functional role of this protein as a determinant of neuronal survival. The general subcellular placement of HSP70 was grossly reported in studies using confocal microscopy, although no direct visualization of this molecule at electron microscopy was carried out. The present study aims to provide a direct evidence of HSP70 within various subcellular compartments. In detail, by using ultrastructural morphometry to quantify HSP70 stoichiometrically detected by immuno-gold within specific organelles we could compare the compartmentalization of the molecule within area penumbra compared with control brain areas. The study indicates that two cell compartments in control conditions own a high density of HSP70, cytosolic vacuoles and mitochondria. In these organelles, HSP70 is present in amount exceeding several-fold the presence in the cytosol. Remarkably, within area penumbra a loss of such a specific polarization is documented. This leads to the depletion of HSP70 from mitochondria and mostly cell vacuoles. Such an effect is expected to lead to significant variations in the ability of HSP70 to exert its physiological roles. The present findings, beyond defining the neuronal compartmentalization of HSP70 within area penumbra may lead to a better comprehension of its beneficial/detrimental role in promoting neuronal survival.


Author(s):  
Tomas T. Roos ◽  
Megg G. Garcia ◽  
Isak Martinsson ◽  
Rana Mabrouk ◽  
Bodil Israelsson ◽  
...  

AbstractThe amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer’s disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.


2015 ◽  
Vol 35 (33) ◽  
pp. 11751-11760 ◽  
Author(s):  
Anthony I. Jang ◽  
Vincent D. Costa ◽  
Peter H. Rudebeck ◽  
Yogita Chudasama ◽  
Elisabeth A. Murray ◽  
...  

2008 ◽  
Vol 53 (5) ◽  
pp. 638-646 ◽  
Author(s):  
Tibor Hajszan ◽  
Neil J. MacLusky ◽  
Csaba Leranth

Glia ◽  
1994 ◽  
Vol 12 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Teresa Gasull ◽  
Mercedes Giralt ◽  
Agustina Garcia ◽  
Juan Hidalgo
Keyword(s):  

2015 ◽  
Vol 67 (5) ◽  
pp. 980-985 ◽  
Author(s):  
Aysu H. Tezcan ◽  
Ayşe Özçetin ◽  
Onur Özlü ◽  
Burcu Çevreli ◽  
Tayfun Uzbay

Author(s):  
Zhen Chen ◽  
Krishnan Padmanabhan

AbstractGrowing evidence shows that top-down projections from excitatory neurons in higher brain areas selectively synapse onto local inhibitory interneurons in sensory systems. While this connectivity is conserved across sensory modalities, the role of this feedback in shaping the dynamics of local circuits, and the resultant computational benefits it provides remains poorly understood. Using rate models of neuronal firing in a network consisting of excitatory, inhibitory and top-down populations, we found that changes in the weight of feedback to inhibitory neurons generated diverse network dynamics and complex transitions between these dynamics. Additionally, modulation of the weight of top-down feedback supported a number of computations, including both pattern separation and oscillatory synchrony. A bifurcation analysis of the network identified a new mechanism by which gamma oscillations could be generated in a model of neural circuits, which we termed Top-down control of Inhibitory Neuron Gamma (TING). We identified the unique roles that top-down feedback of inhibition plays in shaping network dynamics and computation, and the ways in which these dynamics can be deployed to process sensory inputs.Significance StatementThe functional role of feedback projections, connecting excitatory neurons in higher brain areas to inhibitory neurons in primary sensory regions, remains a fundamental open question in neuroscience. Growing evidence suggests that this architecture is recapitulated across a diverse array of sensory systems, ranging from vision to olfaction. Using a rate model of top-down feedback onto inhibition, we found that changes in the weight of feedback support both pattern separation and oscillatory synchrony, including a mechanism by which top-down inputs could entrain gamma oscillations within local networks. These dual functions were accomplished via a codimension-2 bifurcation in the dynamical system. Our results highlight a key role for this top-down feedback, gating inhibition to facilitate often diametrically different local computations.


2020 ◽  
Author(s):  
Thomas Schreiner ◽  
Marit Petzka ◽  
Tobias Staudigl ◽  
Bernhard P. Staresina

ABSTRACTSleep is thought to support memory consolidation via reactivation of prior experiences, with particular electrophysiological sleep signatures (slow oscillations (SOs) and sleep spindles) gating the information flow between relevant brain areas. However, empirical evidence for a role of endogenous memory reactivation (i.e., without experimentally delivered memory cues) for consolidation in humans is lacking. Here, we devised a paradigm in which participants acquired associative memories before taking a nap. Multivariate decoding was then used to capture endogenous memory reactivation during non-rapid eye movement (NREM) sleep. Results revealed reactivation of learning material during SO-spindle complexes, with the precision of SO-spindle coupling predicting reactivation strength. Critically, reactivation strength in turn predicted the level of consolidation across participants. These results elucidate the memory function of sleep in humans and emphasize the importance of SOs and spindles in clocking endogenous consolidation processes.


2021 ◽  
Vol 10 (24) ◽  
pp. 5859
Author(s):  
Katarzyna Wachowska ◽  
Piotr Gałecki

The authors aim to present a narrative review of research on the inflammatory aetiology of depression. Depression is a psychiatric disorder, constituting the most common reason of disability due to a health condition. It has been estimated that at least one in six people suffer from depression at some point of their lives. The aetiology of depression, although researched extensively all around the world, still remains unclear. Authors discuss the possible role of inflammation in depression, the neurodevelopmental theory of depression as well as associations between cognition and depression. Possible associations between memory dysfunction among depressive patients and inflammatory markers are included. The associations between the immune system, depression and cognition are observed. Possible mediating factors between these areas include personality traits, hormonal imbalance and functioning of the brain areas. The question as to what mediating factors are involved is still open to research.


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