Name: synaptic pruning in long-term depression
Uploaded: 2019-03-11T09:21:27.000Z
Duration: 1 min 5 s
Channel: JoVE

Long-term depression, or LTD, is a process of synaptic weakening that occurs over time between pre- and postsynaptic neuronal connections.

One mechanism by which LTD occurs is dependent on the amount of calcium ions flowing into the postsynaptic neuron after presynaptic stimulation. Low calcium concentration due to infrequent presynaptic stimulation can initiate a signaling cascade that culminates in the endocytosis or removal of AMPA glutamate receptors from the membrane. As a result, the postsynaptic response to the same sporadic presynaptic stimulation is further weakened.

Thus, LTD is important for learning, since unused or rarely used synapses are weakened and can even be pruned away, freeing up resources and space that can be used by the neuron for other functions, such as LTP strengthening of more important synapses.

long-term depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity&mdash;changes in the strength of chemical synapses&mdash;can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.

<h4>Calcium Ion Concentration Mechanism</h4>

If over time, all synapses are maximally strengthened through LTP or some other mechanism, the brain would plateau in efficiency making learning and forming new memories difficult. LTD is a way to prune weaker synapses thereby freeing up resources and putting flexibility back into the central nervous system. One mechanism by which LTD occurs depends on the number of calcium ions in the postsynaptic neuron after presynaptic stimulation. Infrequent or low levels of presynaptic stimulation lead to low calcium ion influx and consequently, low calcium ion concentration in the postsynaptic neuron.

The low calcium ion concentration initiates a signaling cascade that culminates in the endocytosis or removal of &alpha;-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors from the plasma membrane. As a result, the postsynaptic response to the same sporadic presynaptic stimulation is further weakened, since there are fewer channels for positively charged ions to enter and depolarize the membrane. The neuron reuses the AMPA receptors at a later time and/or separates them into their constituent subunits.

LTD was first described as occurring in the hippocampus, where it is thought to clear old memories. Subsequently, LTD has been shown to occur in many brain regions such as the cerebellum, striatum, and the cortex. The ubiquitous presence of LTD underlies its importance in proper brain functioning.

<h4>LTD and Disease</h4>

Malfunctioning mechanisms of LTD are thought to contribute to numerous neurological and cognitive disorders such as addiction, mental retardation, and Alzheimer&#39;s disease. Research is ongoing to better understand the mechanisms of LTD, how neurological disorders occur, and to develop treatments.

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity&mdash;changes in the strength of chemical synapses&mdash;can occur in the ...

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synaptic pruning in long-term depression

Long-term depression, or LTD, is a form of synaptic plasticity that weakens chemical synapses over time. It acts between presynaptic and postsynaptic neurons. LTD works in opposition to long-term potentiation, or LTP, which strengthens synapses. Together, LTD and LTP are two of the main mechanisms behind learning and memory.

LTD helps the brain avoid staying locked in a fully strengthened state. If synapses were always maximally strengthened, the brain would become less efficient and it would be harder to learn new information or form new memories. By weakening weaker synapses, LTD helps prune connections and restore flexibility to the central nervous system.

One common LTD mechanism depends on calcium ions in the postsynaptic neuron after presynaptic stimulation. When presynaptic activity is infrequent or low, calcium ion influx is also low. This leads to a low calcium ion concentration in the postsynaptic cell. That signal starts a cascade that removes AMPA glutamate receptors from the plasma membrane through endocytosis.

With fewer AMPA receptors on the membrane, the postsynaptic response to the same weak presynaptic signal becomes even smaller. Fewer channels are available for positively charged ions to enter and depolarize the membrane. The neuron can later reuse these AMPA receptors or break them into subunits.

LTD was first described in the hippocampus, where it is thought to help clear old memories. It has also been found in the cerebellum, striatum, and cortex. Because LTD appears in many brain regions, it is an important part of normal brain function. Problems with LTD are thought to play a role in addiction, mental retardation, and Alzheimer’s disease, so researchers continue to study it and possible treatments.

Synaptic Pruning in Long-term Depression

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Long-term depression, or LTD, is a form of synaptic plasticity that weakens chemical synapses over time. It acts between presynaptic and postsynaptic neurons. LTD works in opposition to long-term potentiation, or LTP, which strengthens synapses. Together, LTD and LTP are two of the main mechanisms behind learning and memory. LTD helps the brain avoid staying locked in a fully strengthened state. If synapses were always maximally strengthened, the brain would become less efficient and it would...

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key terms and concepts

Learn how long-term depression weakens synapses, removes AMPA receptors, and supports learning, memory, and brain flexibility in high school biology.

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Synaptic Pruning in Long-term Depression

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