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Metaplastic
Metaplasticity is a term originally coined by W.C. Abraham and M.F. Bear to refer to the plasticity of synaptic plasticity. Until that time synaptic plasticity had referred to the plastic nature of ''individual'' synapses. However this new form referred to the plasticity of the plasticity itself, thus the term ''meta''-plasticity. The idea is that the synapse's previous history of activity determines its current plasticity. This may play a role in some of the underlying mechanisms thought to be important in memory and learning such as long-term potentiation (LTP), long-term depression (LTD) and so forth. These mechanisms depend on current synaptic "state", as set by ongoing extrinsic influences such as the level of synaptic inhibition, the activity of modulatory afferents such as catecholamines, and the pool of hormones affecting the synapses under study. Recently, it has become clear that the prior history of synaptic activity is an additional variable that influences the synaptic st ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Synaptic Plasticity
In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory (''see Hebbian theory''). Plastic change often results from the alteration of the number of neurotransmitter receptors located on a synapse. There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters. Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon postsynaptic calcium release. Historical discoveries In 1973, Terje Lømo and Tim Bliss first described the now widely studied phenomenon of long-term pote ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Long-term Depression
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress. As the opposing process to long-term potentiation (LTP), LTD is one of several processes that serves to selectively weaken specific synapses in order to make constructive use of synaptic strengthening caused by LTP. This is necessary because, if allowed to continue increasing in strength, synapses would ultimately reach a ceiling level of efficiency, which would inhibit the encoding of new information. Both LTD and LTP are forms of synaptic plasticity. Characterisation LTD in the hippocampus and cerebellum have been the best characterized, but there are other brain areas in which mechanisms of LTD are understood. LTD has also been found to occur in different types of neurons that releas ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Long-term Depression
In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress. As the opposing process to long-term potentiation (LTP), LTD is one of several processes that serves to selectively weaken specific synapses in order to make constructive use of synaptic strengthening caused by LTP. This is necessary because, if allowed to continue increasing in strength, synapses would ultimately reach a ceiling level of efficiency, which would inhibit the encoding of new information. Both LTD and LTP are forms of synaptic plasticity. Characterisation LTD in the hippocampus and cerebellum have been the best characterized, but there are other brain areas in which mechanisms of LTD are understood. LTD has also been found to occur in different types of neurons that releas ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Tenascin-R
Tenascin-R is a protein that in humans is encoded by the ''TNR'' gene. Function Tenascin-R (TNR) is an extracellular matrix protein expressed primarily in the central nervous system. It is a member of the tenascin (TN) gene family, which includes 4 genes in mammals: TNC (or hexabrachion), TNX is a Japanese holding company for various entertainment companies. Its subsidiaries include the talent agency Up-Front Promotion and Up-Front Works, a music production and sales company that manages such record labels as Zetima, Piccolo Town, ... (TNXB), TNW (also known as TNN) and TNR. The genes are expressed in distinct tissues at different times during embryonic development and are present in adult tissues. upplied by OMIMref name="entrez"/> References Further reading * * * * * * * * * * * Tenascins {{gene-1-stub ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Neuroplasticity
Neuroplasticity, also known as neural plasticity, or brain plasticity, is the ability of Neural circuit, neural networks in the brain to change through growth and reorganization. It is when the brain is rewired to function in some way that differs from how it previously functioned. These changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, environmental influences, practice, and psychological stress. Neuroplasticity was once thought by neuroscientists to manifest only during childhood, but research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are "plastic") even through adulthood. However, the developing brain exhibits a higher degree of plasticity than the adult brain. Activity-dependent plasticity can have significant implications for healthy development, le ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Synaptic Tagging
Synaptic tagging, or the synaptic tagging hypothesis, was first proposed in 1997 by Uwe Frey and Richard G. Morris; it seeks to explain how neural signaling at a particular synapse creates a target for subsequent plasticity-related product (PRP) trafficking essential for sustained LTP and LTD. Although the molecular identity of the tags remains unknown, it has been established that they form as a result of high or low frequency stimulation, interact with incoming PRPs, and have a limited lifespan. Further investigations have suggested that plasticity-related products include mRNA and proteins from both the soma and dendritic shaft that must be captured by molecules within the dendritic spine to achieve persistent LTP and LTD. This idea was articulated in the synaptic tag-and-capture hypothesis. Overall, synaptic tagging elaborates on the molecular underpinnings of how L-LTP is generated and leads to memory formation. History Frey, a researcher at the Leibniz Institute f ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Long-term Potentiation
In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength. It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength. As memories are thought to be encoded by modification of synaptic strength, LTP is widely considered one of the major cellular mechanisms that underlies learning and memory. LTP was discovered in the rabbit hippocampus by Terje Lømo in 1966 and has remained a popular subject of research since. Many modern LTP studies seek to better understand its basic biology, while others aim to draw a causal link between LTP and behavioral learning. Still, others try to develop methods, pharmacologic or otherwise, of enhanc ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Silent Synapse
In neuroscience, a silent synapse is an excitatory glutamatergic synapse whose postsynaptic membrane contains NMDA-type glutamate receptors but no AMPA-type glutamate receptors. These synapses are named "silent" because normal AMPA receptor-mediated signaling is not present, rendering the synapse inactive under typical conditions. Silent synapses are typically considered to be immature glutamatergic synapses. As the brain matures, the relative number of silent synapses decreases. However, recent research on hippocampal silent synapses shows that while they may indeed be a developmental landmark in the formation of a synapse, that synapses can be "silenced" by activity, even once they have acquired AMPA receptors. Thus, silence may be a state that synapses can visit many times during their lifetimes. Synaptic transmission Normal transmission across a glutamatergic synapse relies on the neurotransmitter glutamate, the glutamate-specific AMPA receptor (AMPAR), and calcium ions. Ca ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
LTP Induction
The induction of NMDA receptor-dependent long-term potentiation (LTP) in chemical synapses in the brain occurs via a fairly straightforward mechanism. A substantial and rapid rise in calcium ion concentration inside the postsynaptic cell (or more specifically, within the dendritic spine) is most possibly all that is required to induce LTP. But the mechanism of calcium delivery to the postsynaptic cell in inducing LTP is more complicated. The role of the AMPA receptor The AMPA receptor (AMPAR) is the engine that drives excitatory postsynaptic potentials (EPSPs). While some forms of the AMPAR can conduct calcium, most AMPARs found in the neocortex do not. The AMPAR, upon binding two glutamate molecules, undergoes a conformational change that resembles the opening of a clam shell. This conformational change opens an ion channel within the AMPAR protein structure that allows sodium ions to flow into the cell and potassium ions to flow out (i.e. it is a mixed cation-conducting channel). ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
G Protein-coupled Receptor
G protein-coupled receptors (GPCRs), also known as seven-(pass)-transmembrane domain receptors, 7TM receptors, heptahelical receptors, serpentine receptors, and G protein-linked receptors (GPLR), form a large group of evolutionarily-related proteins that are cell surface receptors that detect molecules outside the cell and activate cellular responses. Coupling with G proteins, they are called seven-transmembrane receptors because they pass through the cell membrane seven times. Text was copied from this source, which is available under Attribution 2.5 Generic (CC BY 2.5) license. Ligands can bind either to extracellular N-terminus and loops (e.g. glutamate receptors) or to the binding site within transmembrane helices (Rhodopsin-like family). They are all activated by agonists although a spontaneous auto-activation of an empty receptor can also be observed. G protein-coupled receptors are found only in eukaryotes, including yeast, choanoflagellates, and ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Coincidence Detection In Neurobiology
Coincidence detection in the context of neurobiology is a process by which a neuron or a neural circuit can encode information by detecting the occurrence of temporally close but spatially distributed input signals. Coincidence detectors influence neuronal information processing by reducing temporal jitter, reducing spontaneous activity, and forming associations between separate neural events. This concept has led to a greater understanding of neural processes and the formation of computational maps in the brain. Principles of coincidence detection Coincidence detection relies on separate inputs converging on a common target. Consider a basic neural circuit with two input neurons, A and B, that have excitatory synaptic terminals converging on a single output neuron, C (Fig. 1). If each input neuron's EPSP is subthreshold for an action potential at C, then C will not fire unless the two inputs from A and B are temporally close together. Synchronous arrival of these two inputs m ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Ionotropic Receptor
Ligand-gated ion channels (LICs, LGIC), also commonly referred to as ionotropic receptors, are a group of transmembrane ion-channel proteins which open to allow ions such as Na+, K+, Ca2+, and/or Cl− to pass through the membrane in response to the binding of a chemical messenger (i.e. a ligand), such as a neurotransmitter. When a presynaptic neuron is excited, it releases a neurotransmitter from vesicles into the synaptic cleft. The neurotransmitter then binds to receptors located on the postsynaptic neuron. If these receptors are ligand-gated ion channels, a resulting conformational change opens the ion channels, which leads to a flow of ions across the cell membrane. This, in turn, results in either a depolarization, for an excitatory receptor response, or a hyperpolarization, for an inhibitory response. These receptor proteins are typically composed of at least two different domains: a transmembrane domain which includes the ion pore, and an extracellular domain wh ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
