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Neuronal and Cognitive Plasticity: A Neurocognitive Framework for Ameliorating Cognitive Aging  [PDF]
Pamela M. Greenwood,Raja Parasuraman
Frontiers in Aging Neuroscience , 2010, DOI: 10.3389/fnagi.2010.00150
Abstract: What is the neurocognitive basis for the considerable individual differences observed in functioning of the adult mind and brain late in life? We review the evidence that in healthy old age the brain remains capable of both neuronal and cognitive plasticity, including in response to environmental and experiential factors. Neuronal plasticity (e.g., neurogenesis, synaptogenesis, cortical re-organization) refers to neuron-level changes that can be stimulated by experience. Cognitive plasticity (e.g., increased dependence on executive function) refers to adaptive changes in patterns of cognition related to brain activity. We hypothesize that successful cognitive aging requires interactions between these two forms of plasticity. Mechanisms of neural plasticity underpin cognitive plasticity and in turn, neural plasticity is stimulated by cognitive plasticity. We examine support for this hypothesis by considering evidence that neural plasticity is stimulated by learning and novelty and enhanced by both dietary manipulations (low-fat, dietary restriction) and aerobic exercise. We also examine evidence that cognitive plasticity is affected by education and training. This is a testable hypothesis which could be assessed in humans in randomized trials comparing separate and combined effects of cognitive training, exercise, and diet on measures of cognitive and brain integrity. Greater understanding of the factors influencing the course of cognitive aging and of the mechanisms underlying those factors could provide information on which people could base choices that improve their ability to age successfully.
Linking Neuronal Ensembles by Associative Synaptic Plasticity  [PDF]
Qi Yuan, Jeffry S. Isaacson, Massimo Scanziani
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0020486
Abstract: Synchronized activity in ensembles of neurons recruited by excitatory afferents is thought to contribute to the coding information in the brain. However, the mechanisms by which neuronal ensembles are generated and modified are not known. Here we show that in rat hippocampal slices associative synaptic plasticity enables ensembles of neurons to change by incorporating neurons belonging to different ensembles. Associative synaptic plasticity redistributes the composition of different ensembles recruited by distinct inputs such as to specifically increase the similarity between the ensembles. These results show that in the hippocampus, the ensemble of neurons recruited by a given afferent projection is fluid and can be rapidly and persistently modified to specifically include neurons from different ensembles. This linking of ensembles may contribute to the formation of associative memories.
Error correction and fast detectors implemented by ultra-fast neuronal plasticity  [PDF]
Roni Vardi,Hagar Marmari,Ido Kanter
Quantitative Biology , 2014, DOI: 10.1103/PhysRevE.89.042712
Abstract: We experimentally show that the neuron functions as a precise time-integrator, where the accumulated changes in neuronal response latencies, under complex and random stimulation patterns, are solely a function of a global quantity, the average time-lag between stimulations. In contrast, momentary leaps in the neuronal response latency follow trends of consecutive stimulations, indicating ultra-fast neuronal plasticity. On a circuit level, this ultra-fast neuronal plasticity phenomenon implements error-correction mechanisms and fast detectors for misplaced stimulations. Additionally, at moderate/high stimulation rates this phenomenon destabilizes/stabilizes a periodic neuronal activity disrupted by misplaced stimulations.
Hypothesis on Remote Memory Forming from Heterosynaptic LTD-Mediated Neuronal Degeneration
Zi-Jian Cai
Open Access Library Journal (OALib Journal) , 2019, DOI: 10.4236/oalib.1105442
In this article, it is hypothesized a new mechanism for the formation of stable remote memory in brain comprising the important memory acquired during childhood and the common words in language. It has been demonstrated that the memory forms concurrently at both homosynaptic long term potentiation (LTP) and heterosynaptic long term depression (LTD). It is pointed out that the repeated LTD may result in neuronal degeneration as evidenced at molecular and cellular level, becoming long lasting throughout the lifespan. Besides, it is further supported by the consequent storage of remote memory directly on the information pathway, as evidenced by the degenerative ocular dominance plasticity and the storage of common words/grammar within the linguistic areas of brain. Accordingly, it is herein completed the hypothesis on the formation of remote memory from the heterosynaptic LTD-mediated neuronal degeneration in brain so long as the homosynaptic pathway does not degenerate from such causes as aging and so on, while supplementing a new form of neuronal plasticity for memory in addition to the contemporary LTP and LTD.
Glutamate excitotoxicity: Its correlation with neuronal plasticity in young adults and neonate rats.
Kaur G,Basu A,Kaur AP
Journal of Neurological Sciences , 2003,
Abstract: Although axonal growth in the adult mammalian brain is primarily hampered by adverse environmental conditions, the success of regenerative process is dependent on the capability of injured neurons to express the intrinsic molecular machinery required for neurite elongation. In the present study, regional expression of proteins associated with neuronal and glial growth, such as neural cell adhesion molecule (NCAM), polysialylated neural cell adhesion molecule (PSA-NCAM), Growth-associated protein-43 (GAP-43), Glial fibrillary acidic protein (GFAP) and synaptophysin were studied by immunoblotting technique from different brain regions of monosodium glutamate treated neonate rat pups and young adult rats. The animals were sacrificed after 3 hrs of monosodium glutamate treatment in neonates and 45 days in young adult rats. Control animals were injected with saline alone. NCAM, PSA-NCAM, GFAP and GAP-43 levels were significantly increased in majority of brain regions studied both in neonate and adult group of rats. More pronounced increase in the expression of these markers of neuronal plasticity was observed in the neonate rat pups as compared to young adult animals after monosodium glutamate induced excitotoxicity. These findings support the hypothesis that there is a temporary recapitulation of regenerative state by brain following monosodium glutamate induced CNS injury. Understanding and enhancement of such a response may be one therapeutic strategy in treating CNS injury.
Metabolic Regulation of Neuronal Plasticity by the Energy Sensor AMPK  [PDF]
Wyatt B. Potter,Kenneth J. O'Riordan,David Barnett,Susan M. K. Osting,Matthew Wagoner,Corinna Burger,Avtar Roopra
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008996
Abstract: Long Term Potentiation (LTP) is a leading candidate mechanism for learning and memory and is also thought to play a role in the progression of seizures to intractable epilepsy. Maintenance of LTP requires RNA transcription, protein translation and signaling through the mammalian Target of Rapamycin (mTOR) pathway. In peripheral tissue, the energy sensor AMP-activated Protein Kinase (AMPK) negatively regulates the mTOR cascade upon glycolytic inhibition and cellular energy stress. We recently demonstrated that the glycolytic inhibitor 2-deoxy-D-glucose (2DG) alters plasticity to retard epileptogenesis in the kindling model of epilepsy. Reduced kindling progression was associated with increased recruitment of the nuclear metabolic sensor CtBP to NRSF at the BDNF promoter. Given that energy metabolism controls mTOR through AMPK in peripheral tissue and the role of mTOR in LTP in neurons, we asked whether energy metabolism and AMPK control LTP. Using a combination of biochemical approaches and field-recordings in mouse hippocampal slices, we show that the master regulator of energy homeostasis, AMPK couples energy metabolism to LTP expression. Administration of the glycolytic inhibitor 2-deoxy-D-glucose (2DG) or the mitochondrial toxin and anti-Type II Diabetes drug, metformin, or AMP mimetic AICAR results in activation of AMPK, repression of the mTOR pathway and prevents maintenance of Late-Phase LTP (L-LTP). Inhibition of AMPK by either compound-C or the ATP mimetic ara-A rescues the suppression of L-LTP by energy stress. We also show that enhanced LTP via AMPK inhibition requires mTOR signaling. These results directly link energy metabolism to plasticity in the mammalian brain and demonstrate that AMPK is a modulator of LTP. Our work opens up the possibility of using modulators of energy metabolism to control neuronal plasticity in diseases and conditions of aberrant plasticity such as epilepsy.
Neuronal Plasticity and Multisensory Integration in Filial Imprinting  [PDF]
Stephen Michael Town,Brian John McCabe
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017777
Abstract: Many organisms sample their environment through multiple sensory systems and the integration of multisensory information enhances learning. However, the mechanisms underlying multisensory memory formation and their similarity to unisensory mechanisms remain unclear. Filial imprinting is one example in which experience is multisensory, and the mechanisms of unisensory neuronal plasticity are well established. We investigated the storage of audiovisual information through experience by comparing the activity of neurons in the intermediate and medial mesopallium of imprinted and na?ve domestic chicks (Gallus gallus domesticus) in response to an audiovisual imprinting stimulus and novel object and their auditory and visual components. We find that imprinting enhanced the mean response magnitude of neurons to unisensory but not multisensory stimuli. Furthermore, imprinting enhanced responses to incongruent audiovisual stimuli comprised of mismatched auditory and visual components. Our results suggest that the effects of imprinting on the unisensory and multisensory responsiveness of IMM neurons differ and that IMM neurons may function to detect unexpected deviations from the audiovisual imprinting stimulus.
Spike-timing dependent plasticity beyond synapse - pre- and post-synaptic plasticity of intrinsic neuronal excitability  [PDF]
Dominique Debanne,Mu-Ming Poo
Frontiers in Synaptic Neuroscience , 2010, DOI: 10.3389/fnsyn.2010.00021
Abstract: Long-lasting plasticity of synaptic transmission is classically thought to be the cellular substrate for information storage in the brain. Recent data indicate however that it is not the whole story and persistent changes in the intrinsic neuronal excitability have been shown to occur in parallel to the induction of long-term synaptic modifications. This form of plasticity depends on the regulation of voltage-gated ion channels. Here we review the experimental evidence for plasticity of neuronal excitability induced at pre- or postsynaptic sites when long-term plasticity of synaptic transmission is induced with Spike-Timing Dependent Plasticity (STDP) protocols. We describe the induction and expression mechanisms of the induced changes in excitability. Finally, the functional synergy between synaptic and non-synaptic plasticity and their spatial extent are discussed.
Hypersynchronic Mental Automatisms: An Innovative Psychiatric Hypothesis Reaffirming Its Validity for Fifteen Years  [PDF]
Javier Alvarez-Rodriguez
Health (Health) , 2015, DOI: 10.4236/health.2015.71006
Abstract: This paper deals with certain psychic automatisms that are usually diagnosed as psychiatric symptoms or as simple partial seizures. These mental automatisms are described in many writings by mystics, philosophers, literates, composers, and many different great artists and creators from human history, but they have never conferred any pathological value on these experiences. We have carried out previous scientific researches in which we found abundant arguments suggesting that these automatisms are due to neuronal nets physiologically adapted to fire in a hypersynchronous way. With these pieces of information we propose an audacious hypothesis: these automatic experiences are manifestations of a cognitive cerebral function that, until now, has been insufficiently delimited. We propose the term hyperia to denominate this cognitive function, which we consider responsible for clairvoyant and/or telepathic cognitions. Finally, we discuss the relevant consequences of this hypothesis, particularly in the fields of epilepsy, psychiatry, and neuropsychopharmacology.
DP-b99 Modulates Matrix Metalloproteinase Activity and Neuronal Plasticity  [PDF]
Marine Yeghiazaryan, Izabela Rutkowska-Wlodarczyk, Anna Konopka, Grzegorz M. Wilczyński, Armenuhi Melikyan, Eduard Korkotian, Leszek Kaczmarek, Izabela Figiel
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099789
Abstract: DP-b99 is a membrane-activated chelator of zinc and calcium ions, recently proposed as a therapeutic agent. Matrix metalloproteinases (MMPs) are zinc-dependent extracellularly operating proteases that might contribute to synaptic plasticity, learning and memory under physiological conditions. In excessive amounts these enzymes contribute to a number of neuronal pathologies ranging from the stroke to neurodegeneration and epileptogenesis. In the present study, we report that DP-b99 delays onset and severity of PTZ-induced seizures in mice, as well as displays neuroprotective effect on kainate excitotoxicity in hippocampal organotypic slices and furthermore blocks morphological reorganization of the dendritic spines evoked by a major neuronal MMP, MMP-9. Taken together, our findings suggest that DP-b99 may inhibit neuronal plasticity driven by MMPs, in particular MMP-9, and thus may be considered as a therapeutic agent under conditions of aberrant plasticity, such as those subserving epileptogenesis.
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