Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
10,411
result(s) for
"Plasticity (synaptic)"
Sort by:
Post-stroke cognitive impairment and synaptic plasticity: A review about the mechanisms and Chinese herbal drugs strategies
Post-stroke cognitive impairment, is a major complication of stroke, characterized by cognitive dysfunction, which directly affects the quality of life. Post-stroke cognitive impairment highlights the causal relationship between stroke and cognitive impairment. The pathological damage of stroke, including the increased release of excitatory amino acids, oxidative stress, inflammatory responses, apoptosis, changed neurotrophic factor levels and gene expression, influence synaptic plasticity. Synaptic plasticity refers to the activity-dependent changes in the strength of synaptic connections and efficiency of synaptic transmission at pre-existing synapses and can be divided into structural synaptic plasticity and functional synaptic plasticity. Changes in synaptic plasticity have been proven to play important roles in the occurrence and treatment of post-stroke cognitive impairment. Evidence has indicated that Chinese herbal drugs have effect of treating post-stroke cognitive impairment. In this review, we overview the influence of pathological damage of stroke on synaptic plasticity, analyze the changes of synaptic plasticity in post-stroke cognitive impairment, and summarize the commonly used Chinese herbal drugs whose active ingredient or extracts can regulate synaptic plasticity. This review will summarize the relationship between post-stroke cognitive impairment and synaptic plasticity, provide new ideas for future exploration of the mechanism of post-stroke cognitive impairment, compile evidence of applying Chinese herbal drugs to treat post-stroke cognitive impairment and lay a foundation for the development of novel formulas for treating post-stroke cognitive impairment.
Journal Article
Neuromodulated Spike-Timing-Dependent Plasticity, and Theory of Three-Factor Learning Rules
Classical Hebbian learning puts the emphasis on joint pre- and postsynaptic activity, but neglects the potential role of neuromodulators. Since neuromodulators convey information about novelty or reward, the influence of neuromodulators on synaptic plasticity is useful not just for action learning in classical conditioning, but also to decide \"when\" to create new memories in response to a flow of sensory stimuli. In this review, we focus on timing requirements for pre- and postsynaptic activity in conjunction with one or several phasic neuromodulatory signals. While the emphasis of the text is on conceptual models and mathematical theories, we also discuss some experimental evidence for neuromodulation of Spike-Timing-Dependent Plasticity. We highlight the importance of synaptic mechanisms in bridging the temporal gap between sensory stimulation and neuromodulatory signals, and develop a framework for a class of neo-Hebbian three-factor learning rules that depend on presynaptic activity, postsynaptic variables as well as the influence of neuromodulators.
Journal Article
Synaptic retinoic acid receptor signaling mediates mTOR-dependent metaplasticity that controls hippocampal learning
Homeostatic synaptic plasticity is a stabilizing mechanism engaged by neural circuits in response to prolonged perturbation of network activity. The non-Hebbian nature of homeostatic synaptic plasticity is thought to contribute to network stability by preventing “runaway” Hebbian plasticity at individual synapses. However, whether blocking homeostatic synaptic plasticity indeed induces runaway Hebbian plasticity in an intact neural circuit has not been explored. Furthermore, how compromised homeostatic synaptic plasticity impacts animal learning remains unclear. Here, we show in mice that the experience of an enriched environment (EE) engaged homeostatic synaptic plasticity in hippocampal circuits, thereby reducing excitatory synaptic transmission. This process required RARα, a nuclear retinoic acid receptor that doubles as a cytoplasmic retinoic acid-induced postsynaptic regulator of protein synthesis. Blocking RARα-dependent homeostatic synaptic plasticity during an EE experience by ablating RARα signaling induced runaway Hebbian plasticity, as evidenced by greatly enhanced long-term potentiation (LTP). As a consequence, RARα deletion in hippocampal circuits during an EE experience resulted in enhanced spatial learning but suppressed learning flexibility. In the absence of RARα, moreover, EE experience superactivated mammalian target of rapamycin (mTOR) signaling, causing a shift in protein translation that enhanced the expression levels of AMPA-type glutamate receptors. Treatment of mice with the mTOR inhibitor rapamycin during an EE experience not only restored normal AMPA-receptor expression levels but also reversed the increases in runaway Hebbian plasticity and learning after hippocampal RARα deletion. Thus, our findings reveal an RARα- and mTOR-dependent mechanism by which homeostatic plasticity controls Hebbian plasticity and learning.
Journal Article
Plasmonic Optoelectronic Memristor Enabling Fully Light‐Modulated Synaptic Plasticity for Neuromorphic Vision
Exploration of optoelectronic memristors with the capability to combine sensing and processing functions is required to promote development of efficient neuromorphic vision. In this work, the authors develop a plasmonic optoelectronic memristor that relies on the effects of localized surface plasmon resonance (LSPR) and optical excitation in an Ag–TiO2 nanocomposite film. Fully light‐induced synaptic plasticity (e.g., potentiation and depression) under visible and ultraviolet light stimulations is demonstrated, which enables the functional combination of visual sensing and low‐level image pre‐processing (including contrast enhancement and noise reduction) in a single device. Furthermore, the light‐gated and electrically‐driven synaptic plasticity can be performed in the same device, in which the spike‐timing‐dependent plasticity (STDP) learning functions can be reversibly modulated by visible and ultraviolet light illuminations. Thereby, the high‐level image processing function, i.e., image recognition, can also be performed in this memristor, whose recognition rate and accuracy are obviously enhanced as a result of image pre‐processing and light‐gated STDP enhancement. Experimental analysis shows that the memristive switching mechanism under optical stimulation can be attributed to the oxidation/reduction of Ag nanoparticles due to the effects of LSPR and optical excitation. The authors' work proposes a new type of plasmonic optoelectronic memristor with fully light‐modulated capability that may promote the future development of efficient neuromorphic vision. A novel plasmonic optoelectronic memristor is demonstrated for the first time relying on localized surface plasmon resonance (LSPR) effect. Both fully light‐modulated and light‐gated electrically‐driven synaptic modulation can be implemented in such a single device. Furthermore, combination of visual sensing, low‐level (contrast enhancement and noise reduction), and high‐level image processing (image recognition) promotes the development of efficient neuromorphic vision.
Journal Article
Microtubule-associated protein tau is essential for long-term depression in the hippocampus
The microtubule-associated protein tau is a principal component of neurofibrillary tangles, and has been identified as a key molecule in Alzheimer's disease and other tauopathies. However, it is unknown how a protein that is primarily located in axons is involved in a disease that is believed to have a synaptic origin. To investigate a possible synaptic function of tau, we studied synaptic plasticity in the hippocampus and found a selective deficit in long-term depression (LTD) in tau knockout mice in vivo and in vitro, an effect that was replicated by RNAi knockdown of tau in vitro. We found that the induction of LTD is associated with the glycogen synthase kinase-3-mediated phosphorylation of tau. These observations demonstrate that tau has a critical physiological function in LTD.
Journal Article
biophysically-based neuromorphic model of spike rate- and timing-dependent plasticity
Current advances in neuromorphic engineering have made it possible to emulate complex neuronal ion channel and intracellular ionic dynamics in real time using highly compact and power-efficient complementary metal-oxide-semiconductor (CMOS) analog very-large-scale-integrated circuit technology. Recently, there has been growing interest in the neuromorphic emulation of the spike-timing-dependent plasticity (STDP) Hebbian learning rule by phenomenological modeling using CMOS, memristor or other analog devices. Here, we propose a CMOS circuit implementation of a biophysically grounded neuromorphic (iono-neuromorphic) model of synaptic plasticity that is capable of capturing both the spike rate-dependent plasticity (SRDP, of the Bienenstock-Cooper-Munro or BCM type) and STDP rules. The iono-neuromorphic model reproduces bidirectional synaptic changes with NMDA receptor-dependent and intracellular calcium-mediated long-term potentiation or long-term depression assuming retrograde endocannabinoid signaling as a second coincidence detector. Changes in excitatory or inhibitory synaptic weights are registered and stored in a nonvolatile and compact digital format analogous to the discrete insertion and removal of AMPA or GABA receptor channels. The versatile Hebbian synapse device is applicable to a variety of neuroprosthesis, brain-machine interface, neurorobotics, neuromimetic computation, machine learning, and neural-inspired adaptive control problems.
Journal Article
Synaptotagmin 7 is targeted to the axonal plasma membrane through γ-secretase processing to promote synaptic vesicle docking in mouse hippocampal neurons
Synaptotagmin 7 (SYT7) has emerged as a key regulator of presynaptic function, but its localization and precise role in the synaptic vesicle cycle remain the subject of debate. Here, we used iGluSnFR to optically interrogate glutamate release, at the single-bouton level, in SYT7KO-dissociated mouse hippocampal neurons. We analyzed asynchronous release, paired-pulse facilitation, and synaptic vesicle replenishment and found that SYT7 contributes to each of these processes to different degrees. ‘Zap-and-freeze’ electron microscopy revealed that a loss of SYT7 diminishes docking of synaptic vesicles after a stimulus and inhibits the recovery of depleted synaptic vesicles after a stimulus train. SYT7 supports these functions from the axonal plasma membrane, where its localization and stability require both γ-secretase-mediated cleavage and palmitoylation. In summary, SYT7 is a peripheral membrane protein that controls multiple modes of synaptic vesicle (SV) exocytosis and plasticity, in part, through enhancing activity-dependent docking of SVs.
Journal Article
Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis
A prominent clinical symptom in multiple sclerosis (MS), a progressive disorder of the central nervous system (CNS) due to heightened neuro-inflammation, is learning and memory dysfunction. Here, we investigated the effects of a ketogenic diet (KD) on memory impairment and CNS-inflammation in a murine model of experimental autoimmune encephalomyelitis (EAE), using electrophysiological, behavioral, biochemical and in vivo imaging approaches. Behavioral spatial learning deficits were associated with motor disability in EAE mice, and were observed concurrently with brain inflammation. The KD improved motor disability in the EAE model, as well as CA1 hippocampal synaptic plasticity (long-term potentiation) and spatial learning and memory (assessed with the Morris Water Maze). Moreover, hippocampal atrophy and periventricular lesions in EAE mice were reversed in KD-treated EAE mice. Finally, we found that the increased expression of inflammatory cytokines and chemokines, as well as the production of reactive oxygen species (ROS), in our EAE model were both suppressed by the KD. Collectively, our findings indicate that brain inflammation in EAE mice is associated with impaired spatial learning and memory function, and that KD treatment can exert protective effects, likely via attenuation of the robust immune response and increased oxidative stress seen in these animals.
Journal Article
Scaling of Brain Metabolism with a Fixed Energy Budget per Neuron: Implications for Neuronal Activity, Plasticity and Evolution
It is usually considered that larger brains have larger neurons, which consume more energy individually, and are therefore accompanied by a larger number of glial cells per neuron. These notions, however, have never been tested. Based on glucose and oxygen metabolic rates in awake animals and their recently determined numbers of neurons, here I show that, contrary to the expected, the estimated glucose use per neuron is remarkably constant, varying only by 40% across the six species of rodents and primates (including humans). The estimated average glucose use per neuron does not correlate with neuronal density in any structure. This suggests that the energy budget of the whole brain per neuron is fixed across species and brain sizes, such that total glucose use by the brain as a whole, by the cerebral cortex and also by the cerebellum alone are linear functions of the number of neurons in the structures across the species (although the average glucose consumption per neuron is at least 10× higher in the cerebral cortex than in the cerebellum). These results indicate that the apparently remarkable use in humans of 20% of the whole body energy budget by a brain that represents only 2% of body mass is explained simply by its large number of neurons. Because synaptic activity is considered the major determinant of metabolic cost, a conserved energy budget per neuron has several profound implications for synaptic homeostasis and the regulation of firing rates, synaptic plasticity, brain imaging, pathologies, and for brain scaling in evolution.
Journal Article