Hebbian Ltp
Hebbian Ltp - Related Videos
11:29
Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
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Cited by 52 •
2015
This video article describes experimental procedures to study long-term plasticity and its associative processes such as synaptic tagging, capture and cross-tagging in the CA1 pyramidal neurons using acute hippocampal slices from rodents.
14:57
Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Cited by 62 •
2011
This article outlines procedures for preparing hippocampal slices from rats and transgenic mice for the study of synaptic alterations associated with brain aging and age-related neurodegenerative diseases, such as Alzheimer’s disease.
10:03
Isolation of CA1 Nuclear Enriched Fractions from Hippocampal Slices to Study Activity-dependent Nuclear Import of Synapto-nuclear Messenger Proteins
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Cited by 8 •
2014
We provide a detailed protocol for induction of long-term potentiation in the CA1 region of the hippocampus and the subsequent isolation of nuclear enriched fractions from the tetanized area of the slice. This approach can be used to determine activity dependent nuclear protein import in cellular models of learning and memory.
11:13
Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice
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Cited by 1 •
2013
Transgenic and knockout mouse models of neurological diseases are useful for studying the role of genes in normal and abnormal neurophysiology. This article describes methodologies which can be used to study long-term potentiation, a cellular mechanism which may underlie learning and memory, in transgenic and knockout freely behaving mouse models of neuropathology.
01:05
Long-term Depression
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2019
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—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. Calcium Ion Concentration Mechanism If over time, all...
FAQs
The NMDA receptor’s magnesium block makes postsynaptic depolarization a critical gate in Hebbian LTP. Glutamate released during activity does not complete the strengthening sequence by itself; depolarization relieves the block, allowing calcium to enter. This calcium entry initiates signaling that changes the synapse, linking coordinated electrical activity to increased AMPA receptor contribution.
When connected neurons are activated together, glutamate release and postsynaptic depolarization occur within the same activity pattern. That depolarization relieves the NMDA receptor magnesium block, allowing calcium to enter and activate calcium-dependent signaling. The sequence provides a mechanism through which coordinated neural activity can produce synaptic strengthening.
Calcium-dependent signaling translates NMDA receptor activation into a change in receptor composition at the synapse. After calcium enters, that signaling promotes insertion of AMPA receptors, increasing the receptors available to strengthen synaptic transmission. This step connects the initiating activity pattern with the persistent synaptic modification associated with Hebbian LTP.
Studies focus on hippocampal circuits because they provide a major setting for examining activity-dependent synaptic modification. Researchers can relate repeated or coincident neural activity to the sequence of glutamate release, postsynaptic depolarization, NMDA receptor calcium entry, and AMPA receptor insertion. This circuit-level context connects cellular signaling with questions about learning and memory.
Hebbian LTP offers a cellular framework for studying how experience modifies neural networks. In particular, it supports research into memory formation by connecting patterns of neural activity with strengthened synapses. Its use as a cellular model also helps organize investigations of how changes at individual synapses may contribute to broader effects across neural networks.
The same activity-dependent strengthening framework is relevant beyond memory studies. Research uses Hebbian LTP to examine neural development, where experience-related activity may be linked to changing network connections, and disorders involving altered synaptic plasticity. These applications make the process useful for comparing normal experience-dependent modification with conditions in which synaptic plasticity is disrupted.