LTP Induction
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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). ...
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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 enhanci ...
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Tetanic Stimulation
In neurobiology, a tetanic stimulation consists of a high-frequency sequence of individual stimulations of a neuron. It is associated with potentiation. High-frequency stimulation causes an increase in release called post-tetanic potentiation (Kandel 2003). This presynaptic event is caused by calcium influx. Calcium-protein interactions then produce a change in vesicle exocytosis. The result of these changes is to make the postsynaptic cell more likely to fire an action potential. Tetanic stimulation is used in medicine to detect a non-depolarizing block or a depolarizing block on the neuromuscular junction. Lower elicitations of tetanic stimulation in aged muscles were shown to be caused by lower levels of anaerobic energy provision in skeletal muscles. See also * Hebbian theory Hebbian theory is a neuropsychological theory claiming that an increase in synaptic efficacy arises from a presynaptic cell's repeated and persistent stimulation of a postsynaptic cell. It is an atte ...
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Donald Olding Hebb
Donald Olding Hebb (July 22, 1904 – August 20, 1985) was a Canadian psychologist who was influential in the area of neuropsychology, where he sought to understand how the function of neurons contributed to psychological processes such as learning. He is best known for his theory of Hebbian learning, which he introduced in his classic 1949 work '' The Organization of Behavior''. He has been described as the father of neuropsychology and neural networks. A ''Review of General Psychology'' survey, published in 2002, ranked Hebb as the 19th most cited psychologist of the 20th century. His views on learning described behavior and thought in terms of brain function, explaining cognitive processes in terms of connections between neuron assemblies. Early life Donald Hebb was born in Chester, Nova Scotia, the oldest of four children of Arthur M. and M. Clara (Olding) Hebb, and lived there until the age of 16, when his parents moved to Dartmouth, Nova Scotia. Hebb's parents were both m ...
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Voltage-gated Ion Channel
Voltage-gated ion channels are a class of transmembrane proteins that form ion channels that are activated by changes in a Cell (biology), cell's electrical membrane potential near the channel. The membrane potential alters the conformation of the channel proteins, regulating their opening and closing. Cell membranes are generally impermeable to ions, thus they must diffuse through the membrane through transmembrane protein channels. Voltage-gated ion channels have a crucial role in excitable cells such as neuronal and muscle tissues, allowing a rapid and co-ordinated depolarization in response to triggering Voltage drop, voltage change. Found along the axon and at the synapse, voltage-gated ion channels directionally propagate electrical signals. Voltage-gated ion-channels are usually ion-specific, and channels specific to Sodium channel#Voltage-gated, sodium (Na+), Voltage-gated potassium channel, potassium (K+), Voltage-dependent calcium channel, calcium (Ca2+), and Chloride ...
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Ligand-gated Ion Channel
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 sodium, Na+, potassium, K+, calcium, Ca2+, and/or chloride, Cl− to pass through the membrane in response to the binding of a chemical messenger (i.e. a ligand (biochemistry), 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 (biology), hyperpolarization, for an inhibitory response. These receptor proteins are typically composed of at least two different domains ...
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