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Related Concept Videos

Synaptic Signaling01:09

Synaptic Signaling

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Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
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Synaptic Signaling01:12

Synaptic Signaling

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Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
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Integration of Synaptic Events01:28

Integration of Synaptic Events

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Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
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Long-term Potentiation01:25

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
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Long-term Potentiation01:35

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Chemical Synapses01:26

Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Related Experiment Video

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Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
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Synaptic Signaling in Learning and Memory.

Mary B Kennedy1

  • 1Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, California 91125.

Cold Spring Harbor Perspectives in Biology
|January 1, 2014
PubMed
Summary
This summary is machine-generated.

Synaptic plasticity, crucial for learning and memory, involves altering excitatory synapse strength. This process, initiated postsynaptically, depends on calcium influx and regulates synapse size via receptor changes.

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Synaptic Plasticity

Background:

  • Learning and memory depend on neural network formation.
  • Excitatory synapses, crucial for neural networks, undergo plasticity.
  • Synaptic plasticity modifies synapse strength based on activity patterns.

Purpose of the Study:

  • To elucidate the mechanisms of synaptic plasticity.
  • To understand the role of calcium influx in synaptic strength modulation.
  • To explore the regulation of synapse enlargement and shrinkage.

Main Methods:

  • Investigating postsynaptic mechanisms of synaptic plasticity.
  • Analyzing calcium influx through glutamate receptors.
  • Examining the roles of calcium/calmodulin-regulated enzymes and small GTPases.

Main Results:

  • Synaptic plasticity is initiated in the postsynaptic neuron.
  • Calcium influx patterns dictate receptor addition (LTP) or removal (LTD).
  • Enzymes and GTPases collaborate to control synaptic plasticity.

Conclusions:

  • Synaptic plasticity is a key mechanism for learning and memory.
  • Precise calcium signaling in postsynaptic neurons regulates synapse strength.
  • Calcium-dependent enzymes and GTPases are critical regulators of synaptic plasticity.